A wide scatter of absolute levels of pancreas triacylglycerol has been reported, with a tendency for higher levels in people with diabetes (57). This large population study showed overlap between diabetic and weight-matched control groups. These findings were also observed in a more recent smaller study that used a more precise method (21). Why would one person have normal β-cell function with a pancreas fat level of, for example, 8%, whereas another has type 2 diabetes with a pancreas fat level of 5%? There must be varying degrees of liposusceptibility of the metabolic organs, and this has been demonstrated in relation to ethnic differences (72). If the fat is simply not available to the body, then the susceptibility of the pancreas will not be tested, whereas if the individual acquires excess fat stores, then β-cell failure may or may not develop depending on degree of liposusceptibility. In any group of people with type 2 diabetes, simple inspection reveals that diabetes develops in some with a body mass index (BMI) in the normal or overweight range, whereas others have a very high BMI. The pathophysiologic changes in insulin secretion and insulin sensitivity are not different in obese and normal weight people (73), and the upswing in population rates of type 2 diabetes relates to a right shift in the whole BMI distribution. Hence, the person with a BMI of 24 and type 2 diabetes would in a previous era have had a BMI of 21 and no diabetes. It is clear that individual susceptibility factors determine the onset of the condition, and both genetic and epigenetic factors may contribute. Given that diabetes cannot occur without loss of acute insulin response to food, it can be postulated that this failure of acute insulin secretion could relate to both accumulation of fat and susceptibility to the adverse effect of excess fat in the pancreas.
Glucagon is a hormone that causes the release of glucose from the liver (for example, it promotes gluconeogenesis). Glucagon can be lifesaving and every patient with diabetes who has a history of hypoglycemia (particularly those on insulin) should have a glucagon kit. Families and friends of those with diabetes need to be taught how to administer glucagon, since obviously the patients will not be able to do it themselves in an emergency situation. Another lifesaving device that should be mentioned is very simple; a medic-alert bracelet should be worn by all patients with diabetes.
Diabetes Tracker helps users take control of type 1 and 2 diabetes as well as prediabetes and gestational diabetes. Document exercise and food intake so you can monitor your weight, and view stats and food grades for different foods. It also allows you to keep tabs on water intake, weight, HbA1c, cholesterol, net carbs, and other health factors. Virtual coaching can assist you in managing your health in addition to the analytical tools. This app delivers diabetes management that is truly at your fingertips.
Once nerve damage sets in, your risk of infection increases because you may not be able to feel an injury, like a cut on your foot, to help it heal early on. In addition to examining your feet every day, check in with your doctor at the first sign of infection, such as redness or swelling. Protect your feet by keeping your skin moisturized with a coat of petroleum jelly or rich cream, but make sure to keep the areas between your toes dry because extra moisture there can increase the risk of infection, the ADA suggests.
Since cardiovascular disease is a serious complication associated with diabetes, some have recommended blood pressure levels below 130/80 mmHg.[89] However, evidence supports less than or equal to somewhere between 140/90 mmHg to 160/100 mmHg; the only additional benefit found for blood pressure targets beneath this range was an isolated decrease in stroke risk, and this was accompanied by an increased risk of other serious adverse events.[90][91] A 2016 review found potential harm to treating lower than 140 mmHg.[92] Among medications that lower blood pressure, angiotensin converting enzyme inhibitors (ACEIs) improve outcomes in those with DM while the similar medications angiotensin receptor blockers (ARBs) do not.[93] Aspirin is also recommended for people with cardiovascular problems, however routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes.[94]
In those with impaired glucose tolerance, diet and exercise either alone or in combination with metformin or acarbose may decrease the risk of developing diabetes.[24][70] Lifestyle interventions are more effective than metformin.[24] A 2017 review found that, long term, lifestyle changes decreased the risk by 28%, while medication does not reduce risk after withdrawal.[71] While low vitamin D levels are associated with an increased risk of diabetes, correcting the levels by supplementing vitamin D3 does not improve that risk.[72]
DM occurs when the body cannot produce enough insulin or cannot respond appropriately to insulin. Insulin is a hormone that the body needs to absorb and use glucose (sugar) as fuel for the body’s cells. Without a properly functioning insulin signaling system, blood glucose levels become elevated and other metabolic abnormalities occur, leading to the development of serious, disabling complications.
The word mellitus (/məˈlaɪtəs/ or /ˈmɛlɪtəs/) comes from the classical Latin word mellītus, meaning "mellite"[114] (i.e. sweetened with honey;[114] honey-sweet[115]). The Latin word comes from mell-, which comes from mel, meaning "honey";[114][115] sweetness;[115] pleasant thing,[115] and the suffix -ītus,[114] whose meaning is the same as that of the English suffix "-ite".[116] 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 diabetic had a sweet taste (glycosuria). This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians.

Diabetic hyperglycemic hyperosmolar syndrome (HHS) occurs in type 2 diabetes. It involves very high blood glucose levels but no ketones. You might become dehydrated with this condition. You may even lose consciousness. HHS is most common in people whose diabetes is undiagnosed or who haven’t been able to control their diabetes. It can also be caused by a heart attack, stroke, or infection.
In addition, getting too little sleep can increase your appetite and reduce your level of satiety, causing you to crave carbohydrates and sugary foods, in particular. Over time, indulging in these cravings or overeating, in general, can wreak havoc on your insulin and blood sugar levels, as well as your body weight. (Remember: Obesity is a major risk factor for type 2 diabetes.) Plus, when you’re short on sleep, you’re more likely to feel tired and less inclined to exercise, which is a problem because regular exercise helps with weight management and blood sugar control.
Along with following your diabetes care plan, you may need diabetes medicines, which may include pills or medicines you inject under your skin, such as insulin. Over time, you may need more than one diabetes medicine to manage your blood glucose. Even if you don’t take insulin, you may need it at special times, such as during pregnancy or if you are in the hospital. You also may need medicines for high blood pressure, high cholesterol, or other conditions.
^ Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, Veerman JL, Delwiche K, Iannarone ML, Moyer ML, Cercy K, Vos T, Murray CJ, Forouzanfar MH (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.
A 2018 study suggested that three types should be abandoned as too simplistic.[56] It classified diabetes into five subgroups, with what is typically described as type 1 and autoimmune late-onset diabetes categorized as one group, whereas type 2 encompasses four categories. This is hoped to improve diabetes treatment by tailoring it more specifically to the subgroups.[57]

These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication).

Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.[33][34] The type of fats in the diet are important, with saturated fats and trans fatty acids increasing the risk, and polyunsaturated and monounsaturated fat decreasing the risk.[26] Eating a lot of white rice appears to play a role in increasing risk.[35] A lack of exercise is believed to cause 7% of cases.[36] Persistent organic pollutants may play a role.[37]
Type 2 diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy.[10] This is partly due to a number of complications with which it is associated, including: two to four times the risk of cardiovascular disease, including ischemic heart disease and stroke; a 20-fold increase in lower limb amputations, and increased rates of hospitalizations.[10] In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of nontraumatic blindness and kidney failure.[24] It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia.[25] Other complications include acanthosis nigricans, sexual dysfunction, and frequent infections.[23]
The accepted view has been that the β-cell dysfunction of established diabetes progresses inexorably (79,82,83), whereas insulin resistance can be modified at least to some extent. However, it is now clear that the β-cell defect, not solely hepatic insulin resistance, may be reversible by weight loss at least early in the course of type 2 diabetes (21,84). The low insulin sensitivity of muscle tissue does not change materially either during the onset of diabetes or during subsequent reversal. Overall, the information on the inhibitory effects of excess fat on β-cell function and apoptosis permits a new understanding of the etiology and time course of type 2 diabetes.
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.[108] The term "mellitus" or "from honey" was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus, which is also associated with frequent urination.[108] Effective treatment was not developed until the early part of the 20th century, when Canadians Frederick Banting and Charles Herbert Best isolated and purified insulin in 1921 and 1922.[108] This was followed by the development of the long-acting insulin NPH in the 1940s.[108]

U.S. Department of Health and Human Services. (2014). The health consequences of smoking—50 years of progress: A report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 537–545.
^ Boussageon R, Bejan-Angoulvant T, Saadatian-Elahi M, Lafont S, Bergeonneau C, Kassaï B, Erpeldinger S, Wright JM, Gueyffier F, Cornu C (July 2011). "Effect of intensive glucose lowering treatment on all cause mortality, cardiovascular death, and microvascular events in type 2 diabetes: meta-analysis of randomised controlled trials". BMJ. 343: d4169. doi:10.1136/bmj.d4169. PMC 3144314. PMID 21791495.
The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors.[24][26] While some of these factors are under personal control, such as diet and obesity, other factors are not, such as increasing age, female gender, and genetics.[10] Obesity is more common in women than men in many parts of Africa.[27] A lack of sleep has been linked to type 2 diabetes.[28] This is believed to act through its effect on metabolism.[28] The nutritional status of a mother during fetal development may also play a role, with one proposed mechanism being that of DNA methylation.[29] The intestinal bacteria Prevotella copri and Bacteroides vulgatus have been connected with type 2 diabetes.[30]
When Dan Hamilton was diagnosed with T1D in 1972, the doctor told him he wouldn’t live past 50. Fast forward 45 years, and Dan is strong and healthy at 59. He credits his health to the advancements in treatment and care over the years. He has been an early adopter of every technology that has come along, and exercises regularly as part of a healthy lifestyle.

The prognosis of diabetes is related to the extent to which the condition is kept under control to prevent the development of the complications described in the preceding sections. Some of the more serious complications of diabetes such as kidney failure and cardiovascular disease, can be life-threatening. Acute complications such as diabetic ketoacidosis can also be life-threatening. As mentioned above, aggressive control of blood sugar levels can prevent or delay the onset of complications, and many people with diabetes lead long and full lives.
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
Low blood sugar (hypoglycemia) is common in people with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases.[23][24] Moderately low blood sugar may easily be mistaken for drunkenness;[25] rapid breathing and sweating, cold, pale skin are characteristic of low blood sugar but not definitive.[26] Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.[27]
^ Jump up to: 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): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMC 6350784. PMID 23245607.
You are more likely to develop type 2 diabetes if you are not physically active and are overweight or obese. Extra weight sometimes causes insulin resistance and is common in people with type 2 diabetes. The location of body fat also makes a difference. Extra belly fat is linked to insulin resistance, type 2 diabetes, and heart and blood vessel disease. To see if your weight puts you at risk for type 2 diabetes, check out these Body Mass Index (BMI) charts.