Type 2 diabetes is different. A person with type 2 diabetes still produces insulin but the body doesn't respond to it normally. Glucose is less able to enter the cells and do its job of supplying energy (a problem called insulin resistance). This raises the blood sugar level, so the pancreas works hard to make even more insulin. Eventually, this strain can make the pancreas unable to produce enough insulin to keep blood sugar levels normal.

With gestational diabetes, risks to the unborn baby are even greater than risks to the mother. Risks to the baby include abnormal weight gain before birth, breathing problems at birth, and higher obesity and diabetes risk later in life. Risks to the mother include needing a cesarean section due to an overly large baby, as well as damage to heart, kidney, nerves, and eye.
Every cell in the human body needs energy in order to function. The body's primary energy source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates (sugars and starches). Glucose from the digested food circulates in the blood as a ready energy source for any cells that need it. Insulin is a hormone or chemical produced by cells in the pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to open a doorway into the cell through which glucose can enter. Some of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and saved for later use. When there is not enough insulin produced or when the doorway no longer recognizes the insulin key, glucose stays in the blood rather entering the cells.
You have a higher risk of type 2 diabetes if you are older, have obesity, have a family history of diabetes, or do not exercise. Having prediabetes also increases your risk. Prediabetes means that your blood sugar is higher than normal but not high enough to be called diabetes. If you are at risk for type 2 diabetes, you may be able to delay or prevent developing it by making some lifestyle changes.
According to the National Institutes of Health, the reported rate of gestational diabetes is between 2% to 10% of pregnancies. Gestational diabetes usually resolves itself after pregnancy. Having gestational diabetes does, however, put mothers at risk for developing type 2 diabetes later in life. Up to 10% of women with gestational diabetes develop type 2 diabetes. It can occur anywhere from a few weeks after delivery to months or years later.
There is evidence that certain emotions can promote type 2 diabetes. A recent study found that depression seems to predispose people to diabetes. Other research has tied emotional stress to diabetes, though the link hasn't been proved. Researchers speculate that the emotional connection may have to do with the hormone cortisol, which floods the body during periods of stress. Cortisol sends glucose to the blood, where it can fuel a fight-or-flight response, but overuse of this system may lead to dysfunction.
Diabetes can be looked for by testing a urine sample for sugar but for a diagnosis, a blood sample is required. This may be a simple measurement of the sugar level, usually fasting. Alternatively, a test called an HbA1c can be used which estimates sugar levels over the past couple of months. If someone has typical symptoms of diabetes, only a single abnormal test is required. Where there are no symptoms, a second confirmatory test is required. Sometimes, particularly in pregnancy, a glucose tolerance test is performed which involves blood tests before and 2 hours after a sugary drink.
Although many of the symptoms of type 1 and type 2 diabetes are similar, they present in very different ways. Many people with type 2 diabetes won’t have symptoms for many years. Then often the symptoms of type 2 diabetes develop slowly over the course of time. Some people with type 2 diabetes have no symptoms at all and don’t discover their condition until complications develop.
a chronic metabolic disorder in which the use of carbohydrate is impaired and that of lipid and protein is enhanced. It is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma. Long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
a chronic metabolic disorder in which the use of carbohydrate is impaired and that of lipid and protein is enhanced. It is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma. Long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
Diabetes was one of the first diseases described,[107] with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine".[108] The Ebers papyrus includes a recommendation for a drink to be taken in such cases.[109] The first described cases are believed to be of type 1 diabetes.[108] Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants.[108][109]
DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance
Diet, exercise, and education are the cornerstones of treatment of diabetes and often the first recommendations for people with mild diabetes. Weight loss is important for people who are overweight. People who continue to have elevated blood glucose levels despite lifestyle changes, or have very high blood glucose levels and people with type 1 diabetes (no matter their blood glucose levels) also require drugs.
Diabetes mellitus is a public health problem around the world. In 1980, 108 million adults worldwide had diabetes (4.7% of the global population). By 2014 this had risen to 422 million adults (8.5% of the global population). By 2040, the number is expected to be 642 million adults. In the UK, there is estimated to be between 3 and 4 million people with diabetes. Type 2 diabetes accounts for more than 90% of all patients with diabetes. 

If genetics has taught us anything about diabetes, it's that, for most people, genes aren't the whole story. True, a few rare kinds of diabetes—including those collectively called MODY for maturity-onset diabetes of the young—have been traced to defects in a single gene. But for other types of diabetes, hereditary factors are still not well understood.


DKA usually follows increasing hyperglycemia and symptoms of osmotic diuresis. Users of insulin pumps, by virtue of absent reservoirs of subcutaneous insulin, may present with ketosis and more normal blood glucose levels. They are more likely to present with nausea, vomiting, and abdominal pain, symptoms similar to food poisoning. DKA may manifest as respiratory distress.
A chronic metabolic disorder in which the use of carbohydrate is impaired and that of lipid and protein is enhanced. It is caused by an absolute or relative deficiency of insulin and is characterized, in more severe cases, by chronic hyperglycemia, glycosuria, water and electrolyte loss, ketoacidosis, and coma. Long-term complications include neuropathy, retinopathy, nephropathy, generalized degenerative changes in large and small blood vessels, and increased susceptibility to infection.
In Japan, China, and other Asian countries, the transition from traditional carbohydrate-rich (e.g., rice-based) diets to lower-carbohydrate Westernized eating habits emphasizing meats, dairy products, and fried foods has been accompanied by a major increase in diabetes prevalence. Similarly, in the United States, a meat-based (omnivorous) diet is associated with a high prevalence of diabetes, compared with dietary patterns emphasizing plant-derived foods. In the Adventist Health Study-2, after adjusting for differences in body weight, physical activity, and other factors, an omnivorous diet was associated with roughly double the risk of diabetes, compared with a diet omitting animal products.5
What are the symptoms of diabetes in women? Diabetes can have different effects on men and women. Learn all about the symptoms of diabetes experienced by women with this article, including how the disease may affect pregnancy and the menopause. This MNT Knowledge Center article will also look at gestational diabetes and the risk factors involved. Read now
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