If you are symptomatic (e.g., increased thirst or urination, unexplained weight loss), your doctor may only use a single test to diagnose diabetes/prediabetes. If you don't have any symptoms, one high blood glucose test doesn't necessarily mean you have diabetes/prediabetes. Your doctor will repeat one of the blood tests again on another day (generally 1 week later) to confirm the diagnosis.
In ‘type 2 diabetes’ (previously called non-insulin-dependent diabetes mellitus), which accounts for 90% of all diabetes, the beta cells do not stop making insulin completely, but the insulin produced does not work properly so it struggles to store the sugar found in the blood. As a consequence, the pancreas has to produce more insulin to compensate for this reduction in insulin function. This is called insulin resistance and is commonly linked to obesity. This type of diabetes is seen more commonly over the age of 40 years but can occur at any age.
Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies. These antibodies can be detected in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.
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
Insulin is a hormone made by your pancreas that acts like a key to let blood sugar into the cells in your body for use as energy. If you have type 2 diabetes, cells don’t respond normally to insulin; this is called insulin resistance. Your pancreas makes more insulin to try to get cells to respond. Eventually your pancreas can’t keep up, and your blood sugar rises, setting the stage for prediabetes and type 2 diabetes. High blood sugar is damaging to the body and can cause other serious health problems, such as heart disease, vision loss, and kidney disease.
Can type 2 diabetes be cured? In the early stages of type 2 diabetes, it is possible to manage the diabetes to a level where symptoms go away and A1c reaches a normal level – this effectively “reverses” the progression of type 2 diabetes. According to research from Newcastle University, major weight loss can return insulin secretion to normal in people who had type 2 diabetes for four years or less. Indeed, it is commonly believed that significant weight loss and building muscle mass is the best way to reverse type 2 diabetes progression. However, it is important to note that reversing diabetes progression is not the same as curing type 2 diabetes – people still need to monitor their weight, diet, and exercise to ensure that type 2 diabetes does not progress. For many people who have had type 2 diabetes for a longer time, the damage to the beta cells progresses to the point at which it will never again be possible to make enough insulin to correctly control blood glucose, even with dramatic weight loss. But even in these people, weight loss is likely the best way to reduce the threat of complications.
The most common cause of acquired blindness in many developed nations, diabetic retinopathy is rare in the prepubertal child or within 5 years of onset of diabetes. The prevalence and severity of retinopathy increase with age and are greatest in patients whose diabetic control is poor.  Prevalence rates seem to be declining, yet an estimated 80% of people with type 1 diabetes mellitus develop retinopathy. 
Insulin — the hormone that allows your body to regulate sugar in the blood — is made in your pancreas. Essentially, insulin resistance is a state in which the body’s cells do not use insulin efficiently. As a result, it takes more insulin than normal to transport blood sugar (glucose) into cells, to be used immediately for fuel or stored for later use. A drop in efficiency in getting glucose to cells creates a problem for cell function; glucose is normally the body’s quickest and most readily available source of energy.
Aspirin should be used as secondary prophylaxis in all diabetic people with evidence of macrovascular disease, and it should be strongly considered as primary prevention in diabetic subjects with other risk factors for macrovascular disease, such as hypertension, cigarette smoking, dyslipidemia, obesity, and albuminuria (macro or micro).228 Because of the platelet defects associated with diabetes, it is recommended that the dose of aspirin should be 300 mg per day,228–230 although the American Diabetes Association’s position statement (http://www.diabetes.org/DiabetesCare/supplement198/s45.htm) advocates a dose of 81 to 325 mg enteric-coated aspirin per day. If the patient cannot tolerate aspirin, then clopidogrel231 can be used.
Jump up ^ Imperatore, Giuseppina; Boyle, James P.; Thompson, Theodore J.; Case, Doug; Dabelea, Dana; Hamman, Richard F.; Lawrence, Jean M.; Liese, Angela D.; Liu, Lenna L. (December 2012). "Projections of Type 1 and Type 2 Diabetes Burden in the U.S. Population Aged <20 Years Through 2050". Diabetes Care. 35 (12): 2515–20. doi:10.2337/dc12-0669. ISSN 0149-5992. PMC 3507562. PMID 23173134. Archived from the original on 2016-08-14.
This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.
Type 2 diabetes is most common is those who are genetically predisposed and who are overweight, lead a sedentary lifestyle, have high blood pressure, and/or have insulin resistance due to excess weight. People of certain ethnicities are more likely to develop diabetes, too. These include: African Americans, Mexican Americans, American Indians, Native Hawaiians, Pacific Islanders, and Asian Americans. These populations are more likely to be overweight and have high blood pressure, which increases the risk of developing diabetes.
Abnormal cholesterol and triglyceride levels. If you have low levels of high-density lipoprotein (HDL), or "good," cholesterol, your risk of type 2 diabetes is higher. Triglycerides are another type of fat carried in the blood. People with high levels of triglycerides have an increased risk of type 2 diabetes. Your doctor can let you know what your cholesterol and triglyceride levels are.