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(Redirected from Insulin Deficiency Syndrome)
This article is about the common insulin disorder. For the urine hyper-production disorder, see Diabetes insipidus. For other uses, see Diabetes (disambiguation).

Diabetes mellitus
A hollow circle with a thick blue border and a clear centre
Universal blue circle symbol for diabetes[1]
Pronunciation
SpecialtyEndocrinology
Symptoms
Complications
  • Metabolic imbalances
  • Cardiovascular diseases
  • Nerve and brain damage
  • Kidney failure
  • Gastrointestinal changes[2][3][4][5]
DurationRemission may occur, but diabetes is often life-long
Types
  • Type 1 diabetes
  • Type 2 diabetes
  • Gestational diabetes
CausesInsulin insufficiency or gradual resistance
Risk factors
Diagnostic method
Differential diagnosisdiabetes insipidus
Treatment
Medication
Frequency463 million (5.7%)[9]
Deaths4.2 million (2019)[9]

Diabetes mellitus, often known simply as diabetes, is a group of common endocrine diseases characterized by sustained high blood sugar levels.[10][11] Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body becoming unresponsive to the hormone's effects.[12] Classic symptoms include thirst, polyuria, weight loss, and blurred vision. If left untreated, the disease can lead to various health complications, including disorders of the cardiovascular system, eye, kidney, and nerves.[3] Diabetes accounts for approximately 4.2 million deaths every year,[9] with an estimated 1.5 million caused by either untreated or poorly treated diabetes.[10]

The major types of diabetes are type 1 and type 2.[13] The most common treatment for type 1 is insulin replacement therapy (insulin injections), while anti-diabetic medications (such as metformin and semaglutide) and lifestyle modifications can be used to manage type 2. Gestational diabetes, a form that arises during pregnancy in some women, normally resolves shortly after delivery.

As of 2021, an estimated 537 million people had diabetes worldwide accounting for 10.5% of the adult population, with type 2 making up about 90% of all cases. The World Health Organization has reported that diabetes was "among the top 10 causes of death in 2021, following a significant percentage increase of 95% since 2000."[14] It is estimated that by 2045, approximately 783 million adults, or 1 in 8, will be living with diabetes, representing a 46% increase from the current figures.[15] The prevalence of the disease continues to increase, most dramatically in low- and middle-income nations.[16] Rates are similar in women and men, with diabetes being the seventh leading cause of death globally.[17][18] The global expenditure on diabetes-related healthcare is an estimated US$760 billion a year.[19]

Signs and symptoms

[edit]
Overview of the most significant symptoms of diabetes
Retinopathy, nephropathy, and neuropathy are potential complications of diabetes

The classic symptoms of untreated diabetes are polyuria, thirst, and weight loss.[20] Several other non-specific signs and symptoms may also occur, including fatigue, blurred vision, sweet smelling urine/semen and genital itchiness due to Candida infection.[20] About half of affected individuals may also be asymptomatic.[20] Type 1 presents abruptly following a pre-clinical phase, while type 2 has a more insidious onset; patients may remain asymptomatic for many years.[21]

Diabetic ketoacidosis is a medical emergency that occurs most commonly in type 1, but may also occur in type 2 if it has been longstanding or if the individual has significant β-cell dysfunction.[22] Excessive production of ketone bodies leads to signs and symptoms including nausea, vomiting, abdominal pain, the smell of acetone in the breath, deep breathing known as Kussmaul breathing, and in severe cases decreased level of consciousness.[22] Hyperosmolar hyperglycemic state is another emergency characterized by dehydration secondary to severe hyperglycemia, with resultant hypernatremia leading to an altered mental state and possibly coma.[23]

Hypoglycemia is a recognized complication of insulin treatment used in diabetes.[24] An acute presentation can include mild symptoms such as sweating, trembling, and palpitations, to more serious effects including impaired cognition, confusion, seizures, coma, and rarely death.[24] Recurrent hypoglycemic episodes may lower the glycemic threshold at which symptoms occur, meaning mild symptoms may not appear before cognitive deterioration begins to occur.[24]

Long-term complications

[edit]
Main article: Complications of diabetes

The major long-term complications of diabetes relate to damage to blood vessels at both macrovascular and microvascular levels.[25][26] Diabetes doubles the risk of cardiovascular disease, and about 75% of deaths in people with diabetes are due to coronary artery disease.[27] Other macrovascular morbidities include stroke and peripheral artery disease.[28]

Microvascular disease affects the eyes, kidneys, and nerves.[25] Damage to the retina, known as diabetic retinopathy, is the most common cause of blindness in people of working age.[20] The eyes can also be affected in other ways, including development of cataract and glaucoma.[20] It is recommended that people with diabetes visit an optometrist or ophthalmologist once a year.[29]

Diabetic nephropathy is a major cause of chronic kidney disease, accounting for over 50% of patients on dialysis in the United States.[30] Diabetic neuropathy, damage to nerves, manifests in various ways, including sensory loss, neuropathic pain, and autonomic dysfunction (such as postural hypotension, diarrhoea, and erectile dysfunction).[20] Loss of pain sensation predisposes to trauma that can lead to diabetic foot problems (such as ulceration), the most common cause of non-traumatic lower-limb amputation.[20]

Hearing loss is another long-term complication associated with diabetes.[31]

Based on extensive data and numerous cases of gallstone disease, it appears that a causal link might exist between type 2 diabetes and gallstones. People with diabetes are at a higher risk of developing gallstones compared to those without diabetes.[32]

There is a link between cognitive deficit and diabetes; studies have shown that diabetic individuals are at a greater risk of cognitive decline, and have a greater rate of decline compared to those without the disease.[33] The condition also predisposes to falls in the elderly, especially those treated with insulin.[34]

Causes

[edit]
Comparison of type 1 and 2 diabetes[35]
Feature Type 1 diabetes Type 2 diabetes
Onset Sudden Gradual
Age at onset Any age; average age at diagnosis being 24.[36] Mostly in adults
Body size Thin or normal[37] Often obese
Ketoacidosis Common Rare
Autoantibodies Usually present Absent
Endogenous insulin Low or absent Normal, decreased
or increased
Heritability 0.69 to 0.88[38][39][40] 0.47 to 0.77[41]
Prevalence

(age standardized)

<2 per 1,000[42] ~6% (men), ~5% (women)[43]

Diabetes is classified by the World Health Organization into six categories: type 1 diabetes, type 2 diabetes, hybrid forms of diabetes (including slowly evolving, immune-mediated diabetes of adults and ketosis-prone type 2 diabetes), hyperglycemia first detected during pregnancy, "other specific types", and "unclassified diabetes".[44] Diabetes is a more variable disease than once thought, and individuals may have a combination of forms.[45]

Type 1

[edit]
Main article: Type 1 diabetes

Type 1 accounts for 5 to 10% of diabetes cases and is the most common type diagnosed in patients under 20 years;[46] however, the older term "juvenile-onset diabetes" is no longer used as onset in adulthood is not unusual.[30] The disease is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to severe insulin deficiency, and can be further classified as immune-mediated or idiopathic (without known cause).[46] The majority of cases are immune-mediated, in which a T cell-mediated autoimmune attack causes loss of beta cells and thus insulin deficiency.[47] Patients often have irregular and unpredictable blood sugar levels due to very low insulin and an impaired counter-response to hypoglycemia.[48]

Autoimmune attack in type 1 diabetes.

Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors,[49] such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.[49][50]

Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than a cause.[51] LADA leaves adults with higher levels of insulin production than type 1 diabetes, but not enough insulin production for healthy blood sugar levels.[52][53]

Type 2

[edit]
Main article: Type 2 diabetes
Reduced insulin secretion or weaker effect of insulin on its receptor leads to high glucose content in the blood.

Type 2 diabetes is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion.[12] The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor.[54] However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type of diabetes mellitus accounting for 95% of diabetes.[2] Many people with type 2 diabetes have evidence of prediabetes (impaired fasting glucose and/or impaired glucose tolerance) before meeting the criteria for type 2 diabetes.[55] The progression of prediabetes to overt type 2 diabetes can be slowed or reversed by lifestyle changes or medications that improve insulin sensitivity or reduce the liver's glucose production.[56]

Type 2 diabetes is primarily due to lifestyle factors and genetics.[57] A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than 30), lack of physical activity, poor diet, stress, and urbanization.[35][58] Excess body fat is associated with 30% of cases in people of Chinese and Japanese descent, 60–80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.[12] Even those who are not obese may have a high waist–hip ratio.[12]

Dietary factors such as sugar-sweetened drinks are associated with an increased risk.[59][60] The type of fats in the diet is also important, with saturated fat and trans fats increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk.[57] Eating white rice excessively may increase the risk of diabetes, especially in Chinese and Japanese people.[61] Lack of physical activity may increase the risk of diabetes in some people.[62]

Adverse childhood experiences, including abuse, neglect, and household difficulties, increase the likelihood of type 2 diabetes later in life by 32%, with neglect having the strongest effect.[63]

Antipsychotic medication side effects (specifically metabolic abnormalities, dyslipidemia and weight gain) are also potential risk factors.[64]

Gestational diabetes

[edit]
Main article: Gestational diabetes

Gestational diabetes resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery.[65] It is recommended that all pregnant women get tested starting around 24–28 weeks gestation.[66] It is most often diagnosed in the second or third trimester because of the increase in insulin-antagonist hormone levels that occurs at this time.[66] However, after pregnancy approximately 5–10% of women with gestational diabetes are found to have another form of diabetes, most commonly type 2.[65] Gestational diabetes is fully treatable, but requires careful medical supervision throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases, insulin may be required.[67]

Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital heart and central nervous system abnormalities, and skeletal muscle malformations. Increased levels of insulin in a fetus's blood may inhibit fetal surfactant production and cause infant respiratory distress syndrome. A high blood bilirubin level may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A caesarean section may be performed if there is marked fetal distress[68] or an increased risk of injury associated with macrosomia, such as shoulder dystocia.[69]

Other types

[edit]

Maturity onset diabetes of the young (MODY) is a rare autosomal dominant inherited form of diabetes, due to one of several single-gene mutations causing defects in insulin production.[70] It is significantly less common than the three main types, constituting 1–2% of all cases. The name of this disease refers to early hypotheses as to its nature. Being due to a defective gene, this disease varies in age at presentation and in severity according to the specific gene defect; thus, there are at least 13 subtypes of MODY. People with MODY often can control it without using insulin.[71]

Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells, whereas others increase insulin resistance (especially glucocorticoids which can provoke "steroid diabetes"). The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.[72] Yet another form of diabetes that people may develop is double diabetes. This is when a type 1 diabetic becomes insulin resistant, the hallmark for type 2 diabetes or has a family history for type 2 diabetes.[73] It was first discovered in 1990 or 1991.

The following is a list of disorders that may increase the risk of diabetes:[74]

Pathophysiology

[edit]
The fluctuation of blood sugar (red) and the sugar-lowering hormone insulin (blue) in humans during the course of a day with three meals. One of the effects of a sugar-rich vs a starch-rich meal is highlighted.
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells. Its release is triggered by food, chiefly food containing absorbable glucose.

Insulin is the principal hormone that regulates the uptake of glucose from the blood into most cells of the body, especially liver, adipose tissue and muscle, except smooth muscle, in which insulin acts via the IGF-1.[76] Therefore, deficiency of insulin or the insensitivity of its receptors play a central role in all forms of diabetes mellitus.[77]

The body obtains glucose from three main sources: the intestinal absorption of food; the breakdown of glycogen (glycogenolysis), the storage form of glucose found in the liver; and gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body.[78] Insulin plays a critical role in regulating glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis, it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen.[78]

Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[79]

If the amount of insulin available is insufficient, or if cells respond poorly to the effects of insulin (insulin resistance), or if the insulin itself is defective, then glucose is not absorbed properly by the body cells that require it, and is not stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as metabolic acidosis in cases of complete insulin deficiency.[78]

When there is too much glucose in the blood for a long time, the kidneys cannot absorb it all (reach a threshold of reabsorption) and the extra glucose gets passed out of the body through urine (glycosuria).[80] This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume is replaced osmotically from water in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[78] In addition, intracellular glucose deficiency stimulates appetite leading to excessive food intake (polyphagia).[81]

Diagnosis

[edit]
See also: Glycated hemoglobin and Glucose tolerance test

Diabetes mellitus is diagnosed with a test for the glucose content in the blood, and is diagnosed by demonstrating any one of the following:[72]

  • Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL). For this test, blood is taken after a period of fasting, i.e. in the morning before breakfast, after the patient had sufficient time to fast overnight or at least 8 hours before the test.
  • Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 gram oral glucose load as in a glucose tolerance test (OGTT)
  • Symptoms of high blood sugar and plasma glucose ≥ 11.1 mmol/L (200 mg/dL) either while fasting or not fasting
  • Glycated hemoglobin (HbA1C) ≥ 48 mmol/mol (≥ 6.5 DCCT %).[82]
WHO diabetes diagnostic criteria[83][84]  edit
Condition 2-hour glucose Fasting glucose HbA1c
Unit mmol/L mg/dL mmol/L mg/dL mmol/mol DCCT %
Normal < 7.8 < 140 < 6.1 < 110 < 42 < 6.0
Impaired fasting glycaemia < 7.8 < 140 6.1–7.0 110–125 42–46 6.0–6.4
Impaired glucose tolerance ≥ 7.8 ≥ 140 < 7.0 < 126 42–46 6.0–6.4
Diabetes mellitus ≥ 11.1 ≥ 200 ≥ 7.0 ≥ 126 ≥ 48 ≥ 6.5

A positive result, in the absence of unequivocal high blood sugar, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test.[85] According to the current definition, two fasting glucose measurements at or above 7.0 mmol/L (126 mg/dL) is considered diagnostic for diabetes mellitus.

Per the WHO, people with fasting glucose levels from 6.1 to 6.9 mmol/L (110 to 125 mg/dL) are considered to have impaired fasting glucose.[86] People with plasma glucose at or above 7.8 mmol/L (140 mg/dL), but not over 11.1 mmol/L (200 mg/dL), two hours after a 75 gram oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[87] The American Diabetes Association (ADA) since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/L (100 to 125 mg/dL).[88]

Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.[89]

Prevention

[edit]
See also: Prevention of type 2 diabetes

There is no known preventive measure for type 1 diabetes.[2] However, islet autoimmunity and multiple antibodies can be a strong predictor of the onset of type 1 diabetes.[90] Type 2 diabetes—which accounts for 85–90% of all cases worldwide—can often be prevented or delayed[91] by maintaining a normal body weight, engaging in physical activity, and eating a healthy diet.[2] Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%.[92] Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish.[93] Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes.[93] Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.[94]

The relationship between type 2 diabetes and the main modifiable risk factors (excess weight, unhealthy diet, physical inactivity and tobacco use) is similar in all regions of the world. There is growing evidence that the underlying determinants of diabetes are a reflection of the major forces driving social, economic and cultural change: globalization, urbanization, population aging, and the general health policy environment.[95]

Comorbidity

[edit]

Diabetes patients' comorbidities have a significant impact on medical expenses and related costs. It has been demonstrated that patients with diabetes are more likely to experience respiratory, urinary tract, and skin infections, develop atherosclerosis, hypertension, and chronic kidney disease, putting them at increased risk of infection and complications that require medical attention.[96] Patients with diabetes mellitus are more likely to experience certain infections, such as COVID-19, with prevalence rates ranging from 5.3 to 35.5%.[97][98] Maintaining adequate glycemic control is the primary goal of diabetes management since it is critical to managing diabetes and preventing or postponing such complications.[99]

People with type 1 diabetes have higher rates of autoimmune disorders than the general population. An analysis of a type 1 diabetes registry found that 27% of the 25,000 participants had other autoimmune disorders.[100] Between 2% and 16% of people with type 1 diabetes also have celiac disease.[100]

Management

[edit]
Main article: Diabetes management

Diabetes management concentrates on keeping blood sugar levels close to normal, without causing low blood sugar.[101] This can usually be accomplished with dietary changes,[102] exercise, weight loss, and use of appropriate medications (insulin, oral medications).[101]

Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels.[101][103] The goal of treatment is an A1C level below 7%.[104][105] Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, high blood pressure, metabolic syndrome obesity, and lack of regular exercise.[101][106] Specialized footwear is widely used to reduce the risk of diabetic foot ulcers by relieving the pressure on the foot.[107][108][109] Foot examination for patients living with diabetes should be done annually which includes sensation testing, foot biomechanics, vascular integrity and foot structure.[110]

Concerning those with severe mental illness, the efficacy of type 2 diabetes self-management interventions is still poorly explored, with insufficient scientific evidence to show whether these interventions have similar results to those observed in the general population.[111]

Lifestyle

[edit]
See also: Diet in diabetes

People with diabetes can benefit from education about the disease and treatment, dietary changes, and exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.[112][113]

Weight loss can prevent progression from prediabetes to diabetes type 2, decrease the risk of cardiovascular disease, or result in a partial remission in people with diabetes.[114][115] No single dietary pattern is best for all people with diabetes.[116] Healthy dietary patterns, such as the Mediterranean diet, low-carbohydrate diet, or DASH diet, are often recommended, although evidence does not support one over the others.[114][115] According to the ADA, "reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia", and for individuals with type 2 diabetes who cannot meet the glycemic targets or where reducing anti-glycemic medications is a priority, low or very-low carbohydrate diets are a viable approach.[115] For overweight people with type 2 diabetes, any diet that achieves weight loss is effective.[116][117]

A 2020 Cochrane systematic review compared several non-nutritive sweeteners to sugar, placebo and a nutritive low-calorie sweetener (tagatose), but the results were unclear for effects on HbA1c, body weight and adverse events.[118] The studies included were mainly of very low-certainty and did not report on health-related quality of life, diabetes complications, all-cause mortality or socioeconomic effects.[118]

Exercise has demonstrated to impact people’s lives for a better health outcome. However, fear of hypoglycemia can negatively impact exercise view on youth that have been diagnosed with diabetes. Managing insulin, carbohydrate intake, and physical activity becomes a task that drive youth away benefitting from enjoying exercises. With different studies, an understanding of what can be done and applied to the youth population diagnosed with Type 1 Diabetes has been conducted. A study’s aim was to focus on the impact of an exercise education on physical activity. During the length of a 12-month program, youth and their parents participated in 4 education sessions learning about the benefits, safe procedures, glucose control, and physical activity. With a survey conducted in the beginning, youth and parents demonstrated their fear of hypoglycemia. At the end of the program, most of the youth and parents showed confidence on how to manage and handle situations regarding hypoglycemia. In some instances, youth provided feedback that a continuation of the sessions would be beneficial. In two other studies, exercise was the aim to investigate on how it affects adolescents with T1D. In one of those studies, the impact was assessed in the changes of glucose in exercise by how many minutes per day, intensity, duration, and heart rate. Also, glucose was monitored to see changes during exercise, post exercise, and overnight. The other study investigated how types of exercises can affect glucose levels. The exercise types were continuous moderate exercise and interval-high-intensity exercise. Both types consisted of 2 sets of 10-minute work at different pedaling paces. The continuous pedaled at a 50% and had a 5-minute passive recovery. The high-intensity pedaled at 150% for 15 seconds and was intermixed with a 30-second passive recovery.[119] So, when studies finished collecting data and were able to analyze it, the following were the results. For the studies comparing the different intensities, it was seen that insulin and carbohydrate intake did not have a significant difference before or after exercise. In regards of glucose content, there was a greater drop of blood glucose post exercise in the high intensity (-1.47mmol/L). During recovery, the continuous exercise showed a greater decrease in blood glucose. With all these, continuous exercise resulted in being more favorable for managing blood glucose levels. In the other study, it is mentioned that exercise also contributed to a notable impact on glucose levels. Post-exercise measurements, there was a low mean glucose level that occurred 12 to 16 hours after exercising. Although, with participants exercising for longer sessions (≥90 minutes), hypoglycemia rates were higher. With all these, participants showed well-managed glucose control by intaking proper carbohydrates amount without any insulin adjustments.[120] Lastly, the study, that educated youth and parents about exercise important and management of hypoglycemia, showed many youths feeling confident to continue to exercise regularly and being able to manage their glucose levels.[121] Therefore, as important as exercising is, showing youth and parents that being physical active is possible. That can be done in specific intensities and with proper understanding on how to handle glucose control over time.

Medications

[edit]
Main article: Diabetes medication

Glucose control

[edit]
See also: Anti-diabetic medication

Most medications used to treat diabetes act by lowering blood sugar levels through different mechanisms. There is broad consensus that when people with diabetes maintain tight glucose control – keeping the glucose levels in their blood within normal ranges – they experience fewer complications, such as kidney problems or eye problems.[122][123] There is, however, debate as to whether this is appropriate and cost effective for people later in life in whom the risk of hypoglycemia may be more significant.[124]

There are a number of different classes of anti-diabetic medications. Type 1 diabetes requires treatment with insulin, ideally using a "basal bolus" regimen that most closely matches normal insulin release: long-acting insulin for the basal rate and short-acting insulin with meals.[125] Type 2 diabetes is generally treated with medication that is taken by mouth (e.g. metformin) although some eventually require injectable treatment with insulin or GLP-1 agonists.[126]

Metformin is generally recommended as a first-line treatment for type 2 diabetes, as there is good evidence that it decreases mortality.[7] It works by decreasing the liver's production of glucose, and increasing the amount of glucose stored in peripheral tissue.[127] Several other groups of drugs, mainly oral medication, may also decrease blood sugar in type 2 diabetes. These include agents that increase insulin release (sulfonylureas), agents that decrease absorption of sugar from the intestines (acarbose), agents that inhibit the enzyme dipeptidyl peptidase-4 (DPP-4) that inactivates incretins such as GLP-1 and GIP (sitagliptin), agents that make the body more sensitive to insulin (thiazolidinedione) and agents that increase the excretion of glucose in the urine (SGLT2 inhibitors).[127] When insulin is used in type 2 diabetes, a long-acting formulation is usually added initially, while continuing oral medications.[7]

Some severe cases of type 2 diabetes may also be treated with insulin, which is increased gradually until glucose targets are reached.[7][128]

Blood pressure lowering

[edit]

Cardiovascular disease is a serious complication associated with diabetes, and many international guidelines recommend blood pressure treatment targets that are lower than 140/90 mmHg for people with diabetes.[129] However, there is only limited evidence regarding what the lower targets should be. A 2016 systematic review found potential harm to treating to targets lower than 140 mmHg,[130] and a subsequent systematic review in 2019 found no evidence of additional benefit from blood pressure lowering to between 130 – 140mmHg, although there was an increased risk of adverse events.[131]

2015 American Diabetes Association recommendations are that people with diabetes and albuminuria should receive an inhibitor of the renin-angiotensin system to reduce the risks of progression to end-stage renal disease, cardiovascular events, and death.[132] There is some evidence that angiotensin converting enzyme inhibitors (ACEIs) are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs),[133] or aliskiren in preventing cardiovascular disease.[134] Although a more recent review found similar effects of ACEIs and ARBs on major cardiovascular and renal outcomes.[135] There is no evidence that combining ACEIs and ARBs provides additional benefits.[135]

Aspirin

[edit]

The use of aspirin to prevent cardiovascular disease in diabetes is controversial.[132] Aspirin is recommended by some in people at high risk of cardiovascular disease; however, routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes.[136] 2015 American Diabetes Association recommendations for aspirin use (based on expert consensus or clinical experience) are that low-dose aspirin use is reasonable in adults with diabetes who are at intermediate risk of cardiovascular disease (10-year cardiovascular disease risk, 5–10%).[132] National guidelines for England and Wales by the National Institute for Health and Care Excellence (NICE) recommend against the use of aspirin in people with type 1 or type 2 diabetes who do not have confirmed cardiovascular disease.[125][126]

Surgery

[edit]

Weight loss surgery in those with obesity and type 2 diabetes is often an effective measure.[137] Many are able to maintain normal blood sugar levels with little or no medications following surgery[138] and long-term mortality is decreased.[139] There is, however, a short-term mortality risk of less than 1% from the surgery.[140] The body mass index cutoffs for when surgery is appropriate are not yet clear.[139] It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.[141]

A pancreas transplant is occasionally considered for people with type 1 diabetes who have severe complications of their disease, including end stage kidney disease requiring kidney transplantation.[142]

Diabetic peripheral neuropathy (DPN) affects 30% of all diabetes patients.[143] When DPN is superimposed with nerve compression, DPN may be treatable with multiple nerve decompressions.[144][145] The theory is that DPN predisposes peripheral nerves to compression at anatomical sites of narrowing, and that the majority of DPN symptoms are actually attributable to nerve compression, a treatable condition, rather than DPN itself.[146][147] The surgery is associated with lower pain scores, higher two-point discrimination (a measure of sensory improvement), lower rate of ulcerations, fewer falls (in the case of lower extremity decompression), and fewer amputations.[147][148][149][145]

Self-management and support

[edit]

In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care in a team approach. Evidence has shown that social prescribing led to slight improvements in blood sugar control for people with type 2 diabetes.[150] Home telehealth support can be an effective management technique.[151]

The use of technology to deliver educational programs for adults with type 2 diabetes includes computer-based self-management interventions to collect for tailored responses to facilitate self-management.[152] There is no adequate evidence to support effects on cholesterol, blood pressure, behavioral change (such as physical activity levels and dietary), depression, weight and health-related quality of life, nor in other biological, cognitive or emotional outcomes.[152][153]

Epidemiology

[edit]
Main article: Epidemiology of diabetes
Rates of diabetes worldwide in 2014. The worldwide prevalence was 9.2%.
Mortality rate of diabetes worldwide in 2012 per million inhabitants
  28–91
  92–114
  115–141
  142–163
  164–184
  185–209
  210–247
  248–309
  310–404
  405–1879

In 2017, 425 million people had diabetes worldwide,[154] up from an estimated 382 million people in 2013[155] and from 108 million in 1980.[156] Accounting for the shifting age structure of the global population, the prevalence of diabetes is 8.8% among adults, nearly double the rate of 4.7% in 1980.[154][156] Type 2 makes up about 90% of the cases.[17][35] Some data indicate rates are roughly equal in women and men,[17] but male excess in diabetes has been found in many populations with higher type 2 incidence, possibly due to sex-related differences in insulin sensitivity, consequences of obesity and regional body fat deposition, and other contributing factors such as high blood pressure, tobacco smoking, and alcohol intake.[157][158]

The WHO estimates that diabetes resulted in 1.5 million deaths in 2012, making it the 8th leading cause of death.[159][156] However, another 2.2 million deaths worldwide were attributable to high blood glucose and the increased risks of cardiovascular disease and other associated complications (e.g. kidney failure), which often lead to premature death and are often listed as the underlying cause on death certificates rather than diabetes.[156][160] For example, in 2017, the International Diabetes Federation (IDF) estimated that diabetes resulted in 4.0 million deaths worldwide,[154] using modeling to estimate the total number of deaths that could be directly or indirectly attributed to diabetes.[154]

Diabetes occurs throughout the world but is more common (especially type 2) in more developed countries. The greatest increase in rates has, however, been seen in low- and middle-income countries,[156] where more than 80% of diabetic deaths occur.[161] The fastest prevalence increase is expected to occur in Asia and Africa, where most people with diabetes will probably live in 2030.[162] The increase in rates in developing countries follows the trend of urbanization and lifestyle changes, including increasingly sedentary lifestyles, less physically demanding work and the global nutrition transition, marked by increased intake of foods that are high energy-dense but nutrient-poor (often high in sugar and saturated fats, sometimes referred to as the "Western-style" diet).[156][162] The global number of diabetes cases might increase by 48% between 2017 and 2045.[154]

As of 2020, 38% of all US adults had prediabetes.[163] Prediabetes is an early stage of diabetes.

History

[edit]
Main article: History of diabetes

Diabetes was one of the first diseases described,[164] with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine."[165] The Ebers papyrus includes a recommendation for a drink to take in such cases.[166] The first described cases are believed to have been type 1 diabetes.[165] Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.[165][166]

The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius of Memphis.[165] The disease was considered rare during the time of the Roman empire, with Galen commenting he had only seen two cases during his career.[165] This is possibly due to the diet and lifestyle of the ancients, or because the clinical symptoms were observed during the advanced stage of the disease. Galen named the disease "diarrhea of the urine" (diarrhea urinosa).[167]

The earliest surviving work with a detailed reference to diabetes is that of Aretaeus of Cappadocia (2nd or early 3rd century CE). He described the symptoms and the course of the disease, which he attributed to the moisture and coldness, reflecting the beliefs of the "Pneumatic School". He hypothesized a correlation between diabetes and other diseases, and he discussed differential diagnosis from the snakebite, which also provokes excessive thirst. His work remained unknown in the West until 1552, when the first Latin edition was published in Venice.[167]

Two types of diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 CE with one type being associated with youth and another type with being overweight.[165] Effective treatment was not developed until the early part of the 20th century when Canadians Frederick Banting and Charles Best isolated and purified insulin in 1921 and 1922.[165] This was followed by the development of the long-acting insulin NPH in the 1940s.[165]

Etymology

[edit]

The word diabetes (/ˌdaɪ.əˈbiːtiːz/ or /ˌdaɪ.əˈbiːtɪs/) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon".[168] Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease.[169][170] Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through",[168] which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go".[169] The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.

The word mellitus (/məˈlaɪtəs/ or /ˈmɛlɪtəs/) comes from the classical Latin word mellītus, meaning "mellite"[171] (i.e. sweetened with honey;[171] honey-sweet[172]). The Latin word comes from mell-, which comes from mel, meaning "honey";[171][172] sweetness;[172] pleasant thing,[172] and the suffix -ītus,[171] whose meaning is the same as that of the English suffix "-ite".[173] It was Thomas Willis who in 1675 added "mellitus" to the word "diabetes" as a designation for the disease, when he noticed the urine of a person with diabetes had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, and Indians.[174]

Society and culture

[edit]
Further information: List of films featuring diabetes

The 1989 "St. Vincent Declaration"[175][176] was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important not only in terms of quality of life and life expectancy but also economically – expenses due to diabetes have been shown to be a major drain on health – and productivity-related resources for healthcare systems and governments.

Several countries established more and less successful national diabetes programmes to improve treatment of the disease.[177]

Diabetes stigma

[edit]

Diabetes stigma describes the negative attitudes, judgment, discrimination, or prejudice against people with diabetes. Often, the stigma stems from the idea that diabetes (particularly Type 2 diabetes) resulted from poor lifestyle and unhealthy food choices rather than other causal factors like genetics and social determinants of health.[178] Manifestation of stigma can be seen throughout different cultures and contexts. Scenarios include diabetes statuses affecting marriage proposals, workplace-employment, and social standing in communities.[179]

Stigma is also seen internally, as people with diabetes can also have negative beliefs about themselves. Often these cases of self-stigma are associated with higher diabetes-specific distress, lower self-efficacy, and poorer provider-patient interactions during diabetes care.[180]

Racial and economic inequalities

[edit]

Racial and ethnic minorities are disproportionately affected with higher prevalence of diabetes compared to non-minority individuals.[181] While US adults overall have a 40% chance of developing type 2 diabetes, Hispanic/Latino adults chance is more than 50%.[182] African Americans also are much more likely to be diagnosed with diabetes compared to White Americans. Asians have increased risk of diabetes as diabetes can develop at lower BMI due to differences in visceral fat compared to other races. For Asians, diabetes can develop at a younger age and lower body fat compared to other groups. Additionally, diabetes is highly underreported in Asian American people, as 1 in 3 cases are undiagnosed compared to the average 1 in 5 for the nation.[183]

People with diabetes who have neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to be unemployed as those without the symptoms.[184]

In 2010, diabetes-related emergency room (ER) visit rates in the United States were higher among people from the lowest income communities (526 per 10,000 population) than from the highest income communities (236 per 10,000 population). Approximately 9.4% of diabetes-related ER visits were for the uninsured.[185]

Naming

[edit]

The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus. Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus. Beyond these two types, there is no agreed-upon standard nomenclature.[186]

Diabetes mellitus is also occasionally known as "sugar diabetes" to differentiate it from diabetes insipidus.[187]

Other animals

[edit]
Main articles: Diabetes in dogs and Diabetes in cats

Diabetes can occur in mammals or reptiles.[188][189] Birds do not develop diabetes because of their unusually high tolerance for elevated blood glucose levels.[190]

In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.[191]

Feline diabetes is strikingly similar to human type 2 diabetes. The Burmese, Russian Blue, Abyssinian, and Norwegian Forest cat breeds are at higher risk than other breeds. Overweight cats are also at higher risk.[192]

The symptoms may relate to fluid loss and polyuria, but the course may also be insidious. Diabetic animals are more prone to infections. The long-term complications recognized in humans are much rarer in animals. The principles of treatment (weight loss, oral antidiabetics, subcutaneous insulin) and management of emergencies (e.g. ketoacidosis) are similar to those in humans.[191]

See also

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References

[edit]
  1. ^ "Diabetes Blue Circle Symbol". International Diabetes Federation. 17 March 2006. Archived from the original on 5 August 2007.
  2. ^ a b c d e f g h "Diabetes". www.who.int. Archived from the original on 26 February 2023. Retrieved 1 October 2022.
  3. ^ a b Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (July 2009). "Hyperglycemic crises in adult patients with diabetes". Diabetes Care. 32 (7): 1335–1343. doi:10.2337/dc09-9032. PMC 2699725. PMID 19564476. Archived from the original on 2016-06-25.
  4. ^ Krishnasamy S, Abell TL (July 2018). "Diabetic Gastroparesis: Principles and Current Trends in Management". Diabetes Therapy. 9 (Suppl 1): 1–42. doi:10.1007/s13300-018-0454-9. ISSN 1869-6961. PMC 6028327. PMID 29934758.
  5. ^ Saedi E, Gheini MR, Faiz F, Arami MA (September 2016). "Diabetes mellitus and cognitive impairments". World Journal of Diabetes. 7 (17): 412–422. doi:10.4239/wjd.v7.i17.412. PMC 5027005. PMID 27660698.
  6. ^ a b "Causes of Diabetes – NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. June 2014. Archived from the original on 2 February 2016. Retrieved 10 February 2016.
  7. ^ a b c d Ripsin CM, Kang H, Urban RJ (January 2009). "Management of blood glucose in type 2 diabetes mellitus" (PDF). American Family Physician. 79 (1): 29–36. PMID 19145963. Archived (PDF) from the original on 2013-05-05.
  8. ^ Brutsaert EF (February 2017). "Drug Treatment of Diabetes Mellitus". MSDManuals.com. Archived from the original on 12 October 2018. Retrieved 12 October 2018.
  9. ^ a b c "IDF DIABETES ATLAS Ninth Edition 2019" (PDF). www.diabetesatlas.org. Archived (PDF) from the original on 1 May 2020. Retrieved 18 May 2020.
  10. ^ a b "Diabetes". World Health Organization. Archived from the original on 29 January 2023. Retrieved 29 January 2023.
  11. ^ "Diabetes Mellitus (DM) – Hormonal and Metabolic Disorders". MSD Manual Consumer Version. Archived from the original on 1 October 2022. Retrieved 1 October 2022.
  12. ^ a b c d Shoback DG, Gardner D, eds. (2011). "Chapter 17". Greenspan's basic & clinical endocrinology (9th ed.). New York: McGraw-Hill Medical. ISBN 978-0-07-162243-1.
  13. ^ "Symptoms and Causes of Diabetes". National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 2024. Retrieved 16 May 2024.
  14. ^ "The top 10 causes of death". www.who.int. Retrieved 2024-08-12.
  15. ^ "Facts & figures". International Diabetes Federation. Archived from the original on 2023-08-10. Retrieved 2023-08-10.
  16. ^ De Silva AP, De Silva SH, Haniffa R, Liyanage IK, Jayasinghe S, Katulanda P, et al. (April 2018). "Inequalities in the prevalence of diabetes mellitus and its risk factors in Sri Lanka: a lower middle income country". International Journal for Equity in Health. 17 (1): 45. doi:10.1186/s12939-018-0759-3. PMC 5905173. PMID 29665834.
  17. ^ a b c Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al. (December 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–2196. doi:10.1016/S0140-6736(12)61729-2. PMC 6350784. PMID 23245607.
  18. ^ "The top 10 causes of death". www.who.int. Archived from the original on 24 September 2021. Retrieved 18 May 2020.
  19. ^ Bommer C, Sagalova V, Heesemann E, Manne-Goehler J, Atun R, Bärnighausen T, et al. (May 2018). "Global Economic Burden of Diabetes in Adults: Projections From 2015 to 2030". Diabetes Care. 41 (5): 963–970. doi:10.2337/dc17-1962. PMID 29475843. S2CID 3538441.
  20. ^ a b c d e f g Feather, Adam; Randall, David; Waterhouse, Mona (2021). Kumar and Clark's Clinical Medicine (10th ed.). Elsevier. pp. 699–741. ISBN 978-0-7020-7868-2.
  21. ^ Goldman, Lee; Schafer, Andrew (2020). Goldman-Cecil Medicine (26th ed.). Elsevier. pp. 1490–1510. ISBN 978-0-323-53266-2.
  22. ^ a b Penman, Ian; Ralston, Stuart; Strachan, Mark; Hobson, Richard (2023). Davidson's Principles and Practice of Medicine (24th ed.). Elsevier. pp. 703–753. ISBN 978-0-7020-8348-8.
  23. ^ Willix, Clare; Griffiths, Emma; Singleton, Sally (May 2019). "Hyperglycaemic presentations in type 2 diabetes". Australian Journal of General Practice. 48 (5): 263–267. doi:10.31128/AJGP-12-18-4785. PMID 31129935. S2CID 167207067. Archived from the original on 2023-08-10. Retrieved 2023-08-10.
  24. ^ a b c Amiel, Stephanie A. (2021-05-01). "The consequences of hypoglycaemia". Diabetologia. 64 (5): 963–970. doi:10.1007/s00125-020-05366-3. ISSN 1432-0428. PMC 8012317. PMID 33550443.
  25. ^ a b "Diabetes – long-term effects". Better Health Channel. Victoria: Department of Health. Archived from the original on 2023-10-29. Retrieved 2023-08-12.
  26. ^ Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, et al. (June 2010). "Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies". Lancet. 375 (9733): 2215–2222. doi:10.1016/S0140-6736(10)60484-9. PMC 2904878. PMID 20609967.
  27. ^ O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA, et al. (January 2013). "2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. 127 (4): e368. doi:10.1161/CIR.0b013e3182742cf6. PMID 23247304.
  28. ^ Papatheodorou K, Banach M, Bekiari E, Rizzo M, Edmonds M (11 March 2018). "Complications of Diabetes 2017". Journal of Diabetes Research. 2018: 3086167. doi:10.1155/2018/3086167. PMC 5866895. PMID 29713648.
  29. ^ "Diabetes eye care". MedlinePlus. Maryland: National Library of Medicine. Archived from the original on 2018-03-28. Retrieved 2018-03-27.
  30. ^ a b Wing, Edward J; Schiffman, Fred (2022). Cecil Essentials of Medicine (10th ed.). Pennsylvania: Elsevier. pp. 282–297, 662–677. ISBN 978-0-323-72271-1.
  31. ^ Mittal, Rahul; McKenna, Keelin; Keith, Grant; Lemos, Joana R. N.; Mittal, Jeenu; Hirani, Khemraj (9 February 2024). "A systematic review of the association of Type I diabetes with sensorineural hearing loss". PLOS One. 19 (2): e0298457. Bibcode:2024PLoSO..1998457M. doi:10.1371/journal.pone.0298457. PMC 10857576. PMID 38335215.
  32. ^ Yuan, Shuai; Gill, Dipender; Giovannucci, Edward L.; Larsson, Susanna C. (March 2022). "Obesity, Type 2 Diabetes, Lifestyle Factors, and Risk of Gallstone Disease: A Mendelian Randomization Investigation". Clinical Gastroenterology and Hepatology. 20 (3): e529–e537. doi:10.1016/j.cgh.2020.12.034. hdl:10044/1/86461. PMID 33418132.
  33. ^ Cukierman T, Gerstein HC, Williamson JD (December 2005). "Cognitive decline and dementia in diabetes—systematic overview of prospective observational studies". Diabetologia. 48 (12): 2460–2469. doi:10.1007/s00125-005-0023-4. PMID 16283246.
  34. ^ Yang Y, Hu X, Zhang Q, Zou R (November 2016). "Diabetes mellitus and risk of falls in older adults: a systematic review and meta-analysis". Age and Ageing. 45 (6): 761–767. doi:10.1093/ageing/afw140. PMID 27515679.
  35. ^ a b c Williams textbook of endocrinology (12th ed.). Elsevier/Saunders. 2011. pp. 1371–1435. ISBN 978-1-4377-0324-5.
  36. ^ "Over a Third of Adults With Type 1 Diabetes Weren't Diagnosed Until After 30". U.S. News & World Report. 28 September 2023. Retrieved 3 June 2024.
  37. ^ Lambert P, Bingley PJ (2002). "What is Type 1 Diabetes?". Medicine. 30: 1–5. doi:10.1383/medc.30.1.1.28264.
  38. ^ Skov J, Eriksson D, Kuja-Halkola R, Höijer J, Gudbjörnsdottir S, Svensson AM, et al. (May 2020). "Co-aggregation and heritability of organ-specific autoimmunity: a population-based twin study". European Journal of Endocrinology. 182 (5): 473–480. doi:10.1530/EJE-20-0049. PMC 7182094. PMID 32229696.
  39. ^ Hyttinen V, Kaprio J, Kinnunen L, Koskenvuo M, Tuomilehto J (April 2003). "Genetic liability of type 1 diabetes and the onset age among 22,650 young Finnish twin pairs: a nationwide follow-up study". Diabetes. 52 (4): 1052–1055. doi:10.2337/diabetes.52.4.1052. PMID 12663480.
  40. ^ Condon J, Shaw JE, Luciano M, Kyvik KO, Martin NG, Duffy DL (February 2008). "A study of diabetes mellitus within a large sample of Australian twins" (PDF). Twin Research and Human Genetics. 11 (1): 28–40. doi:10.1375/twin.11.1.28. PMID 18251672. S2CID 18072879. Archived (PDF) from the original on 2023-07-01. Retrieved 2021-12-27.
  41. ^ Willemsen G, Ward KJ, Bell CG, Christensen K, Bowden J, Dalgård C, et al. (December 2015). "The Concordance and Heritability of Type 2 Diabetes in 34,166 Twin Pairs From International Twin Registers: The Discordant Twin (DISCOTWIN) Consortium". Twin Research and Human Genetics. 18 (6): 762–771. doi:10.1017/thg.2015.83. PMID 26678054. S2CID 17854531.
  42. ^ Lin X, Xu Y, Pan X, Xu J, Ding Y, Sun X, et al. (September 2020). "Global, regional, and national burden and trend of diabetes in 195 countries and territories: an analysis from 1990 to 2025". Scientific Reports. 10 (1): 14790. Bibcode:2020NatSR..1014790L. doi:10.1038/s41598-020-71908-9. PMC 7478957. PMID 32901098.
  43. ^ Tinajero MG, Malik VS (September 2021). "An Update on the Epidemiology of Type 2 Diabetes: A Global Perspective". Endocrinology and Metabolism Clinics of North America. 50 (3): 337–355. doi:10.1016/j.ecl.2021.05.013. PMID 34399949.
  44. ^ Classification of diabetes mellitus 2019 (Report). Geneva: World Health Organisation. 2019. ISBN 978-92-4-151570-2. Archived from the original on 2023-03-06. Retrieved 2023-08-15.
  45. ^ Tuomi T, Santoro N, Caprio S, Cai M, Weng J, Groop L (March 2014). "The many faces of diabetes: a disease with increasing heterogeneity". Lancet. 383 (9922): 1084–1094. doi:10.1016/S0140-6736(13)62219-9. PMID 24315621. S2CID 12679248.
  46. ^ a b Kumar, V; Abbas, A; Aster, J (2021). Robbins & Cotran Pathologic Basis of Disease (10th ed.). Pennsylvania: Elsevier. pp. 1065–1132. ISBN 978-0-323-60992-0.
  47. ^ Rother KI (April 2007). "Diabetes treatment—bridging the divide". The New England Journal of Medicine. 356 (15): 1499–1501. doi:10.1056/NEJMp078030. PMC 4152979. PMID 17429082.
  48. ^ Brutsaert, EF (September 2022). "Diabetes Mellitus (DM)". MSD Manual Professional Version. Merck Publishing. Archived from the original on 2023-08-15. Retrieved 2023-08-15.
  49. ^ a b Petzold A, Solimena M, Knoch KP (October 2015). "Mechanisms of Beta Cell Dysfunction Associated With Viral Infection". Current Diabetes Reports (Review). 15 (10): 73. doi:10.1007/s11892-015-0654-x. PMC 4539350. PMID 26280364. So far, none of the hypotheses accounting for virus-induced beta cell autoimmunity has been supported by stringent evidence in humans, and the involvement of several mechanisms rather than just one is also plausible.
  50. ^ Butalia S, Kaplan GG, Khokhar B, Rabi DM (December 2016). "Environmental Risk Factors and Type 1 Diabetes: Past, Present, and Future". Canadian Journal of Diabetes (Review). 40 (6): 586–593. doi:10.1016/j.jcjd.2016.05.002. PMID 27545597.
  51. ^ Laugesen E, Østergaard JA, Leslie RD (July 2015). "Latent autoimmune diabetes of the adult: current knowledge and uncertainty". Diabetic Medicine. 32 (7): 843–852. doi:10.1111/dme.12700. PMC 4676295. PMID 25601320.
  52. ^ "What Is Diabetes?". Diabetes Daily. Archived from the original on 2023-10-04. Retrieved 2023-09-10.
  53. ^ Nolasco-Rosales, Germán Alberto; Ramírez-González, Dania; Rodríguez-Sánchez, Ester; Ávila-Fernandez, Ángela; Villar-Juarez, Guillermo Efrén; González-Castro, Thelma Beatriz; Tovilla-Zárate, Carlos Alfonso; Guzmán-Priego, Crystell Guadalupe; Genis-Mendoza, Alma Delia; Ble-Castillo, Jorge Luis; Marín-Medina, Alejandro; Juárez-Rojop, Isela Esther (2023-04-29). "Identification and phenotypic characterization of patients with LADA in a population of southeast Mexico". Scientific Reports. 13 (1): 7029. Bibcode:2023NatSR..13.7029N. doi:10.1038/s41598-023-34171-2. ISSN 2045-2322. PMC 10148806. PMID 37120620.
  54. ^ Freeman, Andrew M.; Acevedo, Luis A.; Pennings, Nicholas (2024), "Insulin Resistance", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 29939616, archived from the original on 2024-02-07, retrieved 2024-02-13
  55. ^ American Diabetes Association (January 2017). "2. Classification and Diagnosis of Diabetes". Diabetes Care. 40 (Suppl 1): S11–S24. doi:10.2337/dc17-S005. PMID 27979889.
  56. ^ Carris NW, Magness RR, Labovitz AJ (February 2019). "Prevention of Diabetes Mellitus in Patients With Prediabetes". The American Journal of Cardiology. 123 (3): 507–512. doi:10.1016/j.amjcard.2018.10.032. PMC 6350898. PMID 30528418.
  57. ^ a b Risérus U, Willett WC, Hu FB (January 2009). "Dietary fats and prevention of type 2 diabetes". Progress in Lipid Research. 48 (1): 44–51. doi:10.1016/j.plipres.2008.10.002. PMC 2654180. PMID 19032965.
  58. ^ Fletcher, Barbara; Gulanick, Meg; Lamendola, Cindy (January 2002). "Risk factors for type 2 diabetes mellitus". The Journal of Cardiovascular Nursing. 16 (2): 17–23. doi:10.1097/00005082-200201000-00003. ISSN 0889-4655. PMID 11800065. Archived from the original on 2023-10-20. Retrieved 2023-10-12.
  59. ^ Malik VS, Popkin BM, Bray GA, Després JP, Hu FB (March 2010). "Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk". Circulation. 121 (11): 1356–1364. doi:10.1161/CIRCULATIONAHA.109.876185. PMC 2862465. PMID 20308626.
  60. ^ Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB (November 2010). "Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis". Diabetes Care. 33 (11): 2477–2483. doi:10.2337/dc10-1079. PMC 2963518. PMID 20693348.
  61. ^ Hu EA, Pan A, Malik V, Sun Q (March 2012). "White rice consumption and risk of type 2 diabetes: meta-analysis and systematic review". BMJ. 344: e1454. doi:10.1136/bmj.e1454. PMC 3307808. PMID 22422870.
  62. ^ Lee IM, Shiroma EJ, Lobelo F, Puska P, Blair SN, Katzmarzyk PT (July 2012). "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". Lancet. 380 (9838): 219–229. doi:10.1016/S0140-6736(12)61031-9. PMC 3645500. PMID 22818936.
  63. ^ Huang H, Yan P, Shan Z, Chen S, Li M, Luo C, et al. (November 2015). "Adverse childhood experiences and risk of type 2 diabetes: A systematic review and meta-analysis". Metabolism. 64 (11): 1408–1418. doi:10.1016/j.metabol.2015.08.019. PMID 26404480.
  64. ^ Zhang Y, Liu Y, Su Y, You Y, Ma Y, Yang G, et al. (November 2017). "The metabolic side effects of 12 antipsychotic drugs used for the treatment of schizophrenia on glucose: a network meta-analysis". BMC Psychiatry. 17 (1): 373. doi:10.1186/s12888-017-1539-0. PMC 5698995. PMID 29162032.
  65. ^ a b "National Diabetes Clearinghouse (NDIC): National Diabetes Statistics 2011". U.S. Department of Health and Human Services. Archived from the original on 17 April 2014. Retrieved 22 April 2014.
  66. ^ a b Soldavini J (November 2019). "Krause's Food & The Nutrition Care Process". Journal of Nutrition Education and Behavior. 51 (10): 1225. doi:10.1016/j.jneb.2019.06.022. ISSN 1499-4046. S2CID 209272489.
  67. ^ "Managing & Treating Gestational Diabetes | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Archived from the original on 2019-05-06. Retrieved 2019-05-06.
  68. ^ Tarvonen M, Hovi P, Sainio S, Vuorela P, Andersson S, Teramo K (November 2021). "Intrapartal cardiotocographic patterns and hypoxia-related perinatal outcomes in pregnancies complicated by gestational diabetes mellitus". Acta Diabetologica. 58 (11): 1563–1573. doi:10.1007/s00592-021-01756-0. PMC 8505288. PMID 34151398. S2CID 235487220.
  69. ^ National Collaborating Centre for Women's and Children's Health (February 2015). "Intrapartum care". Diabetes in Pregnancy: Management of diabetes and its complications from preconception to the postnatal period. National Institute for Health and Care Excellence (UK). Archived from the original on 2021-08-28. Retrieved 2018-08-21.
  70. ^ "Monogenic Forms of Diabetes". National institute of diabetes and digestive and kidney diseases. US NIH. Archived from the original on 12 March 2017. Retrieved 12 March 2017.
  71. ^ Thanabalasingham G, Owen KR (October 2011). "Diagnosis and management of maturity onset diabetes of the young (MODY)". BMJ. 343 (oct19 3): d6044. doi:10.1136/bmj.d6044. PMID 22012810. S2CID 44891167.
  72. ^ a b "Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications" (PDF). World Health Organization. 1999. Archived (PDF) from the original on 2003-03-08.
  73. ^ Cleland SJ, Fisher BM, Colhoun HM, Sattar N, Petrie JR (July 2013). "Insulin resistance in type 1 diabetes: what is 'double diabetes' and what are the risks?". Diabetologia. 56 (7). National Library of Medicine: 1462–1470. doi:10.1007/s00125-013-2904-2. PMC 3671104. PMID 23613085.
  74. ^ Unless otherwise specified, reference is: Table 20-5 in Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 978-1-4160-2973-1.
  75. ^ Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, et al. (February 2010). "Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials". Lancet. 375 (9716): 735–742. doi:10.1016/S0140-6736(09)61965-6. PMID 20167359. S2CID 11544414.
  76. ^ Wilcox, Gisela (2005-05-05). "Insulin and Insulin Resistance". Clinical Biochemist Reviews. 26 (2): 19–39. ISSN 0159-8090. PMC 1204764. PMID 16278749.
  77. ^ "Insulin Basics". American Diabetes Association. Archived from the original on 21 June 2023. Retrieved 25 June 2023.
  78. ^ a b c d Shoback DG, Gardner D, eds. (2011). Greenspan's basic & clinical endocrinology (9th ed.). McGraw-Hill Medical. ISBN 978-0-07-162243-1.
  79. ^ Barrett KE, et al. (2012). Ganong's review of medical physiology (24th ed.). McGraw-Hill Medical. ISBN 978-0-07-178003-2.
  80. ^ Murray RK, et al. (2012). Harper's illustrated biochemistry (29th ed.). McGraw-Hill Medical. ISBN 978-0-07-176576-3.
  81. ^ Mogotlane S (2013). Juta's Complete Textbook of Medical Surgical Nursing. Cape Town: Juta. p. 839.
  82. ^ "Summary of revisions for the 2010 Clinical Practice Recommendations". Diabetes Care. 33 (Suppl 1): S3. January 2010. doi:10.2337/dc10-S003. PMC 2797388. PMID 20042773. Archived from the original on 13 January 2010. Retrieved 29 January 2010.
  83. ^ Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: Report of a WHO/IDF consultation (PDF). Geneva: World Health Organization. 2006. p. 21. ISBN 978-92-4-159493-6.
  84. ^ Vijan S (March 2010). "In the clinic. Type 2 diabetes". Annals of Internal Medicine. 152 (5): ITC31-15, quiz ITC316. doi:10.7326/0003-4819-152-5-201003020-01003. PMID 20194231.
  85. ^ Saydah SH, Miret M, Sung J, Varas C, Gause D, Brancati FL (August 2001). "Postchallenge hyperglycemia and mortality in a national sample of U.S. adults". Diabetes Care. 24 (8): 1397–1402. doi:10.2337/diacare.24.8.1397. PMID 11473076.
  86. ^ Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: report of a WHO/IDF consultation (PDF). World Health Organization. 2006. p. 21. ISBN 978-92-4-159493-6. Archived (PDF) from the original on 11 May 2012.
  87. ^ Santaguida PL, Balion C, Hunt D, Morrison K, Gerstein H, Raina P, et al. (August 2005). "Diagnosis, prognosis, and treatment of impaired glucose tolerance and impaired fasting glucose". Evidence Report/Technology Assessment (128). Agency for Healthcare Research and Quality: 1–11. PMC 4780988. PMID 16194123. Archived from the original on 16 September 2008. Retrieved 20 July 2008.
  88. ^ Bartoli E, Fra GP, Carnevale Schianca GP (February 2011). "The oral glucose tolerance test (OGTT) revisited". European Journal of Internal Medicine. 22 (1): 8–12. doi:10.1016/j.ejim.2010.07.008. PMID 21238885.
  89. ^ Selvin E, Steffes MW, Zhu H, Matsushita K, Wagenknecht L, Pankow J, et al. (March 2010). "Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults". The New England Journal of Medicine. 362 (9): 800–811. CiteSeerX 10.1.1.589.1658. doi:10.1056/NEJMoa0908359. PMC 2872990. PMID 20200384.
  90. ^ Jacobsen, Laura M.; Haller, Michael J.; Schatz, Desmond A. (2018-03-06). "Understanding Pre-Type 1 Diabetes: The Key to Prevention". Frontiers in Endocrinology. 9: 70. doi:10.3389/fendo.2018.00070. PMC 5845548. PMID 29559955.
  91. ^ "Tackling risk factors for type 2 diabetes in adolescents: PRE-STARt study in Euskadi". Anales de Pediatria. 95 (3). Anales de Pediatría: 186–196. 2020. doi:10.1016/j.anpedi.2020.11.001. PMID 33388268.
  92. ^ Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, et al. (August 2016). "Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013". BMJ. 354: i3857. doi:10.1136/bmj.i3857. PMC 4979358. PMID 27510511.
  93. ^ a b "Simple Steps to Preventing Diabetes". The Nutrition Source. Harvard T.H. Chan School of Public Health. 18 September 2012. Archived from the original on 25 April 2014.
  94. ^ Willi C, Bodenmann P, Ghali WA, Faris PD, Cornuz J (December 2007). "Active smoking and the risk of type 2 diabetes: a systematic review and meta-analysis". JAMA. 298 (22): 2654–2664. doi:10.1001/jama.298.22.2654. PMID 18073361. S2CID 30550981.
  95. ^ "Chronic diseases and their common risk factors" (PDF). World Health Organization. 2005. Archived (PDF) from the original on 2016-10-17. Retrieved 30 August 2016.
  96. ^ CDC (2023-07-31). "Diabetes and Your Immune System". Centers for Disease Control and Prevention. Retrieved 2024-04-25.
  97. ^ Singh, Awadhesh Kumar; Gupta, Ritesh; Ghosh, Amerta; Misra, Anoop (2020). "Diabetes in COVID-19: Prevalence, pathophysiology, prognosis and practical considerations". Diabetes & Metabolic Syndrome. 14 (4): 303–310. doi:10.1016/j.dsx.2020.04.004. ISSN 1878-0334. PMC 7195120. PMID 32298981.
  98. ^ Abdelhafiz, Ahmed H.; Emmerton, Demelza; Sinclair, Alan J. (July 2021). "Diabetes in COVID-19 pandemic-prevalence, patient characteristics and adverse outcomes". International Journal of Clinical Practice. 75 (7): e14112. doi:10.1111/ijcp.14112. ISSN 1742-1241. PMC 7995213. PMID 33630378.
  99. ^ "Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group". Lancet. 352 (9131): 837–853. 1998-09-12. doi:10.1016/S0140-6736(98)07019-6. ISSN 0140-6736. PMID 9742976.
  100. ^ a b Atkinson MA, Mcgill DE, Dassau E, Laffel L (2020). "Type 1 diabetes mellitus". Williams Textbook of Endocrinology. Elsevier. p. 1403.
  101. ^ a b c d "Managing diabetes". National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 1 December 2016. Archived from the original on 6 March 2023. Retrieved 4 February 2023.
  102. ^ Toumpanakis A, Turnbull T, Alba-Barba I (2018-10-30). "Effectiveness of plant-based diets in promoting well-being in the management of type 2 diabetes: a systematic review". BMJ Open Diabetes Research & Care. 6 (1): e000534. doi:10.1136/bmjdrc-2018-000534. PMC 6235058. PMID 30487971.
  103. ^ The Diabetes Control and Complications Trial Research Group (April 1995). "The effect of intensive diabetes therapy on the development and progression of neuropathy". Annals of Internal Medicine. 122 (8): 561–568. doi:10.7326/0003-4819-122-8-199504150-00001. PMID 7887548. S2CID 24754081.
  104. ^ "The A1C test and diabetes". National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health. 1 April 2018. Archived from the original on 4 February 2023. Retrieved 4 February 2023.
  105. ^ Qaseem A, Wilt TJ, Kansagara D, et al. (April 2018). "Hemoglobin A1c Targets for Glycemic Control With Pharmacologic Therapy for Nonpregnant Adults With Type 2 Diabetes Mellitus: A Guidance Statement Update From the American College of Physicians". Annals of Internal Medicine. 168 (8): 569–576. doi:10.7326/M17-0939. PMID 29507945.
  106. ^ National Institute for Health and Clinical Excellence. Clinical guideline 66: Type 2 diabetes. London, 2008.
  107. ^ Bus SA, van Deursen RW, Armstrong DG, Lewis JE, Caravaggi CF, Cavanagh PR (January 2016). "Footwear and offloading interventions to prevent and heal foot ulcers and reduce plantar pressure in patients with diabetes: a systematic review". Diabetes/Metabolism Research and Reviews. 32 (Suppl 1): 99–118. doi:10.1002/dmrr.2702. PMID 26342178. S2CID 24862853.
  108. ^ Heuch L, Streak Gomersall J (July 2016). "Effectiveness of offloading methods in preventing primary diabetic foot ulcers in adults with diabetes: a systematic review". JBI Database of Systematic Reviews and Implementation Reports. 14 (7): 236–265. doi:10.11124/JBISRIR-2016-003013. PMID 27532798. S2CID 12012686.
  109. ^ van Netten JJ, Raspovic A, Lavery LA, Monteiro-Soares M, Rasmussen A, Sacco IC, Bus SA (March 2020). "Prevention of foot ulcers in the at-risk patient with diabetes: a systematic review" (PDF). Diabetes/Metabolism Research and Reviews. 36 (S1 Suppl 1): e3270. doi:10.1002/dmrr.3270. PMID 31957213. S2CID 210830578. Archived (PDF) from the original on 2023-02-09. Retrieved 2023-01-23.
  110. ^ Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM (January 2004). "Preventive foot care in diabetes". Diabetes Care. 27 (suppl_1): S63–S64. doi:10.2337/diacare.27.2007.S63. PMID 14693928.
  111. ^ McBain H, Mulligan K, Haddad M, Flood C, Jones J, Simpson A, et al. (Cochrane Metabolic and Endocrine Disorders Group) (April 2016). "Self management interventions for type 2 diabetes in adult people with severe mental illness". The Cochrane Database of Systematic Reviews. 2016 (4): CD011361. doi:10.1002/14651858.CD011361.pub2. PMC 10201333. PMID 27120555.
  112. ^ Haw JS, Galaviz KI, Straus AN, et al. (December 2017). "Long-term Sustainability of Diabetes Prevention Approaches: A Systematic Review and Meta-analysis of Randomized Clinical Trials". JAMA Internal Medicine. 177 (12): 1808–1817. doi:10.1001/jamainternmed.2017.6040. PMC 5820728. PMID 29114778.
  113. ^ Mottalib A, Kasetty M, Mar JY, Elseaidy T, Ashrafzadeh S, Hamdy O (August 2017). "Weight Management in Patients with Type 1 Diabetes and Obesity". Current Diabetes Reports. 17 (10): 92. doi:10.1007/s11892-017-0918-8. PMC 5569154. PMID 28836234.
  114. ^ a b American Diabetes Association (January 2019). "5. Lifestyle Management: Standards of Medical Care in Diabetes-2019". Diabetes Care. 42 (Suppl 1): S46–S60. doi:10.2337/dc19-S005. PMID 30559231.
  115. ^ a b c Evert AB, Dennison M, Gardner CD, et al. (May 2019). "Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report". Diabetes Care (Professional society guidelines). 42 (5): 731–754. doi:10.2337/dci19-0014. PMC 7011201. PMID 31000505.
  116. ^ a b Emadian A, Andrews RC, England CY, Wallace V, Thompson JL (November 2015). "The effect of macronutrients on glycaemic control: a systematic review of dietary randomised controlled trials in overweight and obese adults with type 2 diabetes in which there was no difference in weight loss between treatment groups". The British Journal of Nutrition. 114 (10): 1656–1666. doi:10.1017/S0007114515003475. PMC 4657029. PMID 26411958.
  117. ^ Grams J, Garvey WT (June 2015). "Weight Loss and the Prevention and Treatment of Type 2 Diabetes Using Lifestyle Therapy, Pharmacotherapy, and Bariatric Surgery: Mechanisms of Action". Current Obesity Reports. 4 (2): 287–302. doi:10.1007/s13679-015-0155-x. PMID 26627223. S2CID 207474124.
  118. ^ a b Lohner, Szimonetta; Kuellenberg de Gaudry, Daniela; Toews, Ingrid; Ferenci, Tamas; Meerpohl, Joerg J (2020-05-25). Cochrane Metabolic and Endocrine Disorders Group (ed.). "Non-nutritive sweeteners for diabetes mellitus". Cochrane Database of Systematic Reviews. 2020 (5): CD012885. doi:10.1002/14651858.CD012885.pub2. PMC 7387865. PMID 32449201.
  119. ^ Parent, Cassandra; Lespagnol, Elodie; Berthoin, Serge; Tagougui, Sémah; Stuckens, Chantal; Tonoli, Cajsa; Dupire, Michelle; Dewaele, Aline; Dereumetz, Julie; Dewast, Chloé; Gueorgieva, Iva; Rabasa-Lhoret, Rémi; Heyman, Elsa (April 2024). "Continuous moderate and intermittent high-intensity exercise in youth with type 1 diabetes: Which protection for dysglycemia?". Diabetes Research and Clinical Practice. 210: 111631. doi:10.1016/j.diabres.2024.111631. ISSN 0168-8227.
  120. ^ Sherr, Jennifer L.; Bergford, Simon; Gal, Robin L.; Clements, Mark A.; Patton, Susana R.; Calhoun, Peter; Beaulieu, Lindsey C.; Riddell, Michael C. (2024-05-01). "Exploring Factors That Influence Postexercise Glycemia in Youth With Type 1 Diabetes in the Real World: The Type 1 Diabetes Exercise Initiative Pediatric (T1DEXIP) Study". Diabetes Care. 47 (5): 849–857. doi:10.2337/dc23-2212. ISSN 0149-5992.
  121. ^ Tanenbaum, Molly L.; Addala, Ananta; Hanes, Sarah; Ritter, Victor; Bishop, Franziska K.; Cortes, Ana L.; Pang, Erica; Hood, Korey K.; Maahs, David M.; Zaharieva, Dessi P. (2024-01-01). ""It changed everything we do": A mixed methods study of youth and parent experiences with a pilot exercise education intervention following new diagnosis of type 1 diabetes". Journal of Diabetes and its Complications. 38 (1): 108651. doi:10.1016/j.jdiacomp.2023.108651. ISSN 1056-8727. PMC 10843536. PMID 38043358.
  122. ^ Rosberger DF (December 2013). "Diabetic retinopathy: current concepts and emerging therapy". Endocrinology and Metabolism Clinics of North America. 42 (4): 721–745. doi:10.1016/j.ecl.2013.08.001. PMID 24286948.
  123. ^ MacIsaac RJ, Jerums G, Ekinci EI (March 2018). "Glycemic Control as Primary Prevention for Diabetic Kidney Disease". Advances in Chronic Kidney Disease. 25 (2): 141–148. doi:10.1053/j.ackd.2017.11.003. PMID 29580578.
  124. ^ Pozzilli P, Strollo R, Bonora E (March 2014). "One size does not fit all glycemic targets for type 2 diabetes". Journal of Diabetes Investigation. 5 (2): 134–141. doi:10.1111/jdi.12206. PMC 4023573. PMID 24843750.
  125. ^ a b "Type 1 diabetes in adults: diagnosis and management". www.nice.org.uk. National Institute for Health and Care Excellence. 26 August 2015. Archived from the original on 10 December 2020. Retrieved 25 December 2020.
  126. ^ a b "Type 2 diabetes in adults: management". www.nice.org.uk. National Institute for Health and Care Excellence. 2 December 2015. Archived from the original on 22 December 2020. Retrieved 25 December 2020.
  127. ^ a b Krentz AJ, Bailey CJ (2005). "Oral antidiabetic agents: current role in type 2 diabetes mellitus". Drugs. 65 (3): 385–411. doi:10.2165/00003495-200565030-00005. PMID 15669880. S2CID 29670619.
  128. ^ Consumer Reports; American College of Physicians (April 2012), "Choosing a type 2 diabetes drug – Why the best first choice is often the oldest drug" (PDF), High Value Care, Consumer Reports, archived (PDF) from the original on July 2, 2014, retrieved August 14, 2012
  129. ^ Mitchell S, Malanda B, Damasceno A, et al. (September 2019). "A Roadmap on the Prevention of Cardiovascular Disease Among People Living With Diabetes". Global Heart. 14 (3): 215–240. doi:10.1016/j.gheart.2019.07.009. PMID 31451236.
  130. ^ Brunström M, Carlberg B (February 2016). "Effect of antihypertensive treatment at different blood pressure levels in patients with diabetes mellitus: systematic review and meta-analyses". BMJ. 352: i717. doi:10.1136/bmj.i717. PMC 4770818. PMID 26920333.
  131. ^ Brunström M, Carlberg B (September 2019). "Benefits and harms of lower blood pressure treatment targets: systematic review and meta-analysis of randomised placebo-controlled trials". BMJ Open. 9 (9): e026686. doi:10.1136/bmjopen-2018-026686. PMC 6773352. PMID 31575567.
  132. ^ a b c Fox CS, Golden SH, Anderson C, et al. (September 2015). "Update on Prevention of Cardiovascular Disease in Adults With Type 2 Diabetes Mellitus in Light of Recent Evidence: A Scientific Statement From the American Heart Association and the American Diabetes Association". Diabetes Care. 38 (9): 1777–1803. doi:10.2337/dci15-0012. PMC 4876675. PMID 26246459.
  133. ^ Cheng J, Zhang W, Zhang X, et al. (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–785. doi:10.1001/jamainternmed.2014.348. PMID 24687000.
  134. ^ Zheng SL, Roddick AJ, Ayis S (September 2017). "Effects of aliskiren on mortality, cardiovascular outcomes and adverse events in patients with diabetes and cardiovascular disease or risk: A systematic review and meta-analysis of 13,395 patients". Diabetes & Vascular Disease Research. 14 (5): 400–406. doi:10.1177/1479164117715854. PMC 5600262. PMID 28844155.
  135. ^ a b Catalá-López F, Macías Saint-Gerons D, González-Bermejo D, et al. (March 2016). "Cardiovascular and Renal Outcomes of Renin-Angiotensin System Blockade in Adult Patients with Diabetes Mellitus: A Systematic Review with Network Meta-Analyses". PLOS Medicine. 13 (3): e1001971. doi:10.1371/journal.pmed.1001971. PMC 4783064. PMID 26954482.
  136. ^ Pignone M, Alberts MJ, Colwell JA, et al. (June 2010). "Aspirin for primary prevention of cardiovascular events in people with diabetes: a position statement of the American Diabetes Association, a scientific statement of the American Heart Association, and an expert consensus document of the American College of Cardiology Foundation". Diabetes Care. 33 (6): 1395–1402. doi:10.2337/dc10-0555. PMC 2875463. PMID 20508233.
  137. ^ Picot J, Jones J, Colquitt JL, Gospodarevskaya E, Loveman E, Baxter L, Clegg AJ (September 2009). "The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: a systematic review and economic evaluation". Health Technology Assessment. 13 (41): 1–190, 215–357, iii–iv. doi:10.3310/hta13410. hdl:10536/DRO/DU:30064294. PMID 19726018.
  138. ^ Frachetti KJ, Goldfine AB (April 2009). "Bariatric surgery for diabetes management". Current Opinion in Endocrinology, Diabetes and Obesity. 16 (2): 119–124. doi:10.1097/MED.0b013e32832912e7. PMID 19276974. S2CID 31797748.
  139. ^ a b Schulman AP, del Genio F, Sinha N, Rubino F (September–October 2009). ""Metabolic" surgery for treatment of type 2 diabetes mellitus". Endocrine Practice. 15 (6): 624–631. doi:10.4158/EP09170.RAR. PMID 19625245.
  140. ^ Colucci RA (January 2011). "Bariatric surgery in patients with type 2 diabetes: a viable option". Postgraduate Medicine. 123 (1): 24–33. doi:10.3810/pgm.2011.01.2242. PMID 21293081. S2CID 207551737.
  141. ^ Dixon JB, le Roux CW, Rubino F, Zimmet P (June 2012). "Bariatric surgery for type 2 diabetes". Lancet. 379 (9833): 2300–2311. doi:10.1016/S0140-6736(12)60401-2. PMID 22683132. S2CID 5198462.
  142. ^ "Pancreas Transplantation". American Diabetes Association. Archived from the original on 13 April 2014. Retrieved 9 April 2014.
  143. ^ Sun J, Wang Y, Zhang X, Zhu S, He H (October 2020). "Prevalence of peripheral neuropathy in patients with diabetes: A systematic review and meta-analysis". Prim Care Diabetes. 14 (5): 435–444. doi:10.1016/j.pcd.2019.12.005. PMID 31917119.
  144. ^ Xu L, Sun Z, Casserly E, Nasr C, Cheng J, Xu J (June 2022). "Advances in Interventional Therapies for Painful Diabetic Neuropathy: A Systematic Review". Anesth Analg. 134 (6): 1215–1228. doi:10.1213/ANE.0000000000005860. PMC 9124666. PMID 35051958.
  145. ^ a b Tu Y, Lineaweaver WC, Chen Z, Hu J, Mullins F, Zhang F (March 2017). "Surgical Decompression in the Treatment of Diabetic Peripheral Neuropathy: A Systematic Review and Meta-analysis". J Reconstr Microsurg. 33 (3): 151–157. doi:10.1055/s-0036-1594300. PMID 27894152.
  146. ^ Dellon AL (February 1988). "A cause for optimism in diabetic neuropathy". Ann Plast Surg. 20 (2): 103–5. doi:10.1097/00000637-198802000-00001. PMID 3355053.
  147. ^ a b Sessions J, Nickerson DS (March 2014). "Biologic Basis of Nerve Decompression Surgery for Focal Entrapments in Diabetic Peripheral Neuropathy". J Diabetes Sci Technol. 8 (2): 412–418. doi:10.1177/1932296814525030. PMC 4455405. PMID 24876595.
  148. ^ Fadel ZT, Imran WM, Azhar T (August 2022). "Lower Extremity Nerve Decompression for Diabetic Peripheral Neuropathy: A Systematic Review and Meta-analysis". Plast Reconstr Surg Glob Open. 10 (8): e4478. doi:10.1097/GOX.0000000000004478. PMC 9390809. PMID 35999882.
  149. ^ Xu L, Sun Z, Casserly E, Nasr C, Cheng J, Xu J (June 2022). "Advances in Interventional Therapies for Painful Diabetic Neuropathy: A Systematic Review". Anesth Analg. 134 (6): 1215–1228. doi:10.1213/ANE.0000000000005860. PMC 9124666. PMID 35051958.
  150. ^ "Can social prescribing improve the health of people with diabetes?". National Institute for Health and Care Research – NIHR Evidence. 2024. doi:10.3310/nihrevidence_61876. S2CID 267264134. Archived from the original on 26 January 2024. Retrieved 26 January 2024.
  151. ^ Polisena J, Tran K, Cimon K, Hutton B, McGill S, Palmer K (October 2009). "Home telehealth for diabetes management: a systematic review and meta-analysis". Diabetes, Obesity & Metabolism. 11 (10): 913–930. doi:10.1111/j.1463-1326.2009.01057.x. PMID 19531058. S2CID 44260857.
  152. ^ a b Pal K, Eastwood SV, Michie S, et al. (Cochrane Metabolic and Endocrine Disorders Group) (March 2013). "Computer-based diabetes self-management interventions for adults with type 2 diabetes mellitus". The Cochrane Database of Systematic Reviews. 2013 (3): CD008776. doi:10.1002/14651858.CD008776.pub2. PMC 6486319. PMID 23543567.
  153. ^ Wei I, Pappas Y, Car J, Sheikh A, Majeed A, et al. (Cochrane Metabolic and Endocrine Disorders Group) (December 2011). "Computer-assisted versus oral-and-written dietary history taking for diabetes mellitus". The Cochrane Database of Systematic Reviews. 2011 (12): CD008488. doi:10.1002/14651858.CD008488.pub2. PMC 6486022. PMID 22161430.
  154. ^ a b c d e Elflein J (10 December 2019). Estimated number diabetics worldwide. Archived from the original on 29 July 2020. Retrieved 17 May 2020.
  155. ^ Shi Y, Hu FB (June 2014). "The global implications of diabetes and cancer". Lancet. 383 (9933): 1947–1948. doi:10.1016/S0140-6736(14)60886-2. PMID 24910221. S2CID 7496891.
  156. ^ a b c d e f "Global Report on Diabetes" (PDF). World Health Organization. 2016. Archived (PDF) from the original on 16 May 2018. Retrieved 20 September 2018.
  157. ^ Gale EA, Gillespie KM (January 2001). "Diabetes and gender". Diabetologia. 44 (1): 3–15. doi:10.1007/s001250051573. PMID 11206408.
  158. ^ Meisinger C, Thorand B, Schneider A, Stieber J, Döring A, Löwel H (January 2002). "Sex differences in risk factors for incident type 2 diabetes mellitus: the MONICA Augsburg cohort study". Archives of Internal Medicine. 162 (1): 82–89. doi:10.1001/archinte.162.1.82. PMID 11784224.
  159. ^ "The top 10 causes of death Fact sheet N°310". World Health Organization. October 2013. Archived from the original on 30 May 2017.
  160. ^ Public Health Agency of Canada, Diabetes in Canada: Facts and figures from a public health perspective. Ottawa, 2011.
  161. ^ Mathers CD, Loncar D (November 2006). "Projections of global mortality and burden of disease from 2002 to 2030". PLOS Medicine. 3 (11): e442. doi:10.1371/journal.pmed.0030442. PMC 1664601. PMID 17132052.
  162. ^ a b Wild S, Roglic G, Green A, Sicree R, King H (May 2004). "Global prevalence of diabetes: estimates for the year 2000 and projections for 2030". Diabetes Care. 27 (5): 1047–1053. doi:10.2337/diacare.27.5.1047. PMID 15111519.
  163. ^ "Prevalence of Prediabetes Among Adults – Diabetes". CDC. 2018-03-13. Archived from the original on 2023-03-06. Retrieved 2022-12-15.
  164. ^ Ripoll BC, Leutholtz I (2011-04-25). Exercise and disease management (2nd ed.). Boca Raton: CRC Press. p. 25. ISBN 978-1-4398-2759-8. Archived from the original on 2016-04-03.
  165. ^ a b c d e f g h Poretsky L, ed. (2009). Principles of diabetes mellitus (2nd ed.). New York: Springer. p. 3. ISBN 978-0-387-09840-1. Archived from the original on 2016-04-04.
  166. ^ a b Roberts J (2015). "Sickening sweet". Distillations. Vol. 1, no. 4. pp. 12–15. Archived from the original on 13 November 2019. Retrieved 20 March 2018.
  167. ^ a b Laios K, Karamanou M, Saridaki Z, Androutsos G (2012). "Aretaeus of Cappadocia and the first description of diabetes" (PDF). Hormones. 11 (1): 109–113. doi:10.1007/BF03401545. PMID 22450352. S2CID 4730719. Archived (PDF) from the original on 2017-01-04.
  168. ^ a b Oxford English Dictionary. diabetes. Retrieved 2011-06-10.
  169. ^ a b Harper D (2001–2010). "Online Etymology Dictionary. diabetes.". Archived from the original on 2012-01-13. Retrieved 2011-06-10.
  170. ^ Aretaeus, De causis et signis acutorum morborum (lib. 2), Κεφ. β. περὶ Διαβήτεω (Chapter 2, On Diabetes, Greek original) Archived 2014-07-02 at the Wayback Machine, on Perseus
  171. ^ a b c d Oxford English Dictionary. mellite. Retrieved 2011-06-10.
  172. ^ a b c d "MyEtimology. mellitus.". Archived from the original on 2011-03-16. Retrieved 2011-06-10.{{cite web}}: CS1 maint: unfit URL (link)
  173. ^ Oxford English Dictionary. -ite. Retrieved 2011-06-10.
  174. ^ Guthrie, Diana W. (1988). "Diabetes Urine Testing: An Historical Perspective". The Diabetes Educator. 14 (6): 521–525. doi:10.1177/014572178801400615. PMID 3061764.
  175. ^ Tulchinsky TH, Varavikova EA (2008). The New Public Health, Second Edition. New York: Academic Press. p. 200. ISBN 978-0-12-370890-8.
  176. ^ Piwernetz K, Home PD, Snorgaard O, Antsiferov M, Staehr-Johansen K, Krans M (May 1993). "Monitoring the targets of the St Vincent Declaration and the implementation of quality management in diabetes care: the DIABCARE initiative. The DIABCARE Monitoring Group of the St Vincent Declaration Steering Committee". Diabetic Medicine. 10 (4): 371–377. doi:10.1111/j.1464-5491.1993.tb00083.x. PMID 8508624. S2CID 9931183.
  177. ^ Dubois H, Bankauskaite V (2005). "Type 2 diabetes programmes in Europe" (PDF). Euro Observer. 7 (2): 5–6. Archived (PDF) from the original on 2012-10-24.
  178. ^ CDC (2022-11-03). "Diabetes Stigma: Learn About It, Recognize It, Reduce It". Centers for Disease Control and Prevention. Archived from the original on 2023-10-31. Retrieved 2023-10-31.
  179. ^ Schabert, Jasmin; Browne, Jessica L.; Mosely, Kylie; Speight, Jane (2013-03-01). "Social Stigma in Diabetes". The Patient – Patient-Centered Outcomes Research. 6 (1): 1–10. doi:10.1007/s40271-012-0001-0. ISSN 1178-1661. PMID 23322536. S2CID 207490680.
  180. ^ Puhl, Rebecca M.; Himmelstein, Mary S.; Hateley-Browne, Jessica L.; Speight, Jane (October 2020). "Weight stigma and diabetes stigma in U.S. adults with type 2 diabetes: Associations with diabetes self-care behaviors and perceptions of health care". Diabetes Research and Clinical Practice. 168: 108387. doi:10.1016/j.diabres.2020.108387. ISSN 0168-8227. PMID 32858100. S2CID 221366068.
  181. ^ Spanakis, Elias K.; Golden, Sherita Hill (December 2013). "Race/Ethnic Difference in Diabetes and Diabetic Complications". Current Diabetes Reports. 13 (6): 10.1007/s11892–013–0421–9. doi:10.1007/s11892-013-0421-9. ISSN 1534-4827. PMC 3830901. PMID 24037313.
  182. ^ CDC (2022-04-04). "Hispanic/Latino Americans and Type 2 Diabetes". Centers for Disease Control and Prevention. Archived from the original on 2023-10-31. Retrieved 2023-10-31.
  183. ^ CDC (2022-11-21). "Diabetes and Asian American People". Centers for Disease Control and Prevention. Archived from the original on 2023-10-31. Retrieved 2023-10-31.
  184. ^ Stewart WF, Ricci JA, Chee E, Hirsch AG, Brandenburg NA (June 2007). "Lost productive time and costs due to diabetes and diabetic neuropathic pain in the US workforce". Journal of Occupational and Environmental Medicine. 49 (6): 672–679. doi:10.1097/JOM.0b013e318065b83a. PMID 17563611. S2CID 21487348.
  185. ^ Washington R.E.; Andrews R.M.; Mutter R.L. (November 2013). "Emergency Department Visits for Adults with Diabetes, 2010". HCUP Statistical Brief (167). Rockville MD: Agency for Healthcare Research and Quality. PMID 24455787. Archived from the original on 2013-12-03.
  186. ^ "Type 1 vs. Type 2 Diabetes Differences: Which One Is Worse?". MedicineNet. Archived from the original on 2021-04-14. Retrieved 2021-03-21.
  187. ^ Parker K (2008). Living with diabetes. New York: Facts On File. p. 143. ISBN 978-1-4381-2108-6.
  188. ^ Niaz K, Maqbool F, Khan F, Hassan FI, Momtaz S, Abdollahi M (April 2018). "Comparative occurrence of diabetes in canine, feline, and few wild animals and their association with pancreatic diseases and ketoacidosis with therapeutic approach". Veterinary World. 11 (4): 410–422. doi:10.14202/vetworld.2018.410-422. PMC 5960778. PMID 29805204.
  189. ^ Stahl SJ (2006-01-01). "Hyperglycemia in Reptiles". In Mader DR (ed.). Reptile Medicine and Surgery (Second ed.). Saint Louis: W.B. Saunders. pp. 822–830. doi:10.1016/b0-72-169327-x/50062-6. ISBN 978-0-7216-9327-9.
  190. ^ Sweazea KL (8 July 2022). "Revisiting glucose regulation in birds - A negative model of diabetes complications". Comparative Biochemistry and Physiology. Part B, Biochemistry & Molecular Biology. 262: 110778. doi:10.1016/j.cbpb.2022.110778. PMID 35817273. S2CID 250404382.
  191. ^ a b "Diabetes mellitus". Merck Veterinary Manual (9th ed.). 2005. Archived from the original on 2011-09-27. Retrieved 2011-10-23.
  192. ^ Öhlund M. Feline diabetes mellitus Aspects on epidemiology and pathogenesis (PDF). Acta Universitatis agriculturae Sueciae. ISBN 978-91-7760-067-1. Archived (PDF) from the original on 2021-04-13. Retrieved 2017-12-18.
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