Often people don't experience symptoms of diabetes until their blood sugars are very high. Symptoms of diabetes include: increased thirst, increased urination, increased hunger, extreme fatigues, numbness and tingling in the extremities (hands and feet), cuts and wounds that are slow to heal, and blurred vision. Some people also experience other less common symptoms including weight loss, dry itchy skin, increased yeast infections, erectile dysfunction, and acanthosis nigricans (thick, "velvety" patches found in the folds or creases of skin, such as the neck, that is indicative of insulin resistance).
A study by Chan et al indicated that in pediatric patients with type 1 diabetes, the presence of hypoglycemia is a sign of decreased insulin sensitivity, while hyperglycemia in these patients, especially overnight, signals improved sensitivity to insulin. In contrast, the investigators found evidence that in pediatric patients with type 2 diabetes, markers of metabolic syndrome and hyperglycemia are associated with reduced insulin sensitivity. Patients in the study were between ages 12 and 19 years. [23]
Oral medications are available to lower blood glucose in Type II diabetics. In 1990, 23.4 outpatient prescriptions for oral antidiabetic agents were dispensed. By 2001, the number had increased to 91.8 million prescriptions. Oral antidiabetic agents accounted for more than $5 billion dollars in worldwide retail sales per year in the early twenty-first century and were the fastest-growing segment of diabetes drugs. The drugs first prescribed for Type II diabetes are in a class of compounds called sulfonylureas and include tolbutamide, tolazamide, acetohexamide, and chlorpropamide. Newer drugs in the same class are now available and include glyburide, glimeperide, and glipizide. How these drugs work is not well understood, however, they seem to stimulate cells of the pancreas to produce more insulin. New medications that are available to treat diabetes include metformin, acarbose, and troglitizone. The choice of medication depends in part on the individual patient profile. All drugs have side effects that may make them inappropriate for particular patients. Some for example, may stimulate weight gain or cause stomach irritation, so they may not be the best treatment for someone who is already overweight or who has stomach ulcers. Others, like metformin, have been shown to have positive effects such as reduced cardiovascular mortality, but but increased risk in other situations. While these medications are an important aspect of treatment for Type II diabetes, they are not a substitute for a well planned diet and moderate exercise. Oral medications have not been shown effective for Type I diabetes, in which the patient produces little or no insulin.
Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known ones above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.[23]
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
Glycated hemoglobin (A1C) test. This blood test indicates your average blood sugar level for the past two to three months. It measures the percentage of blood sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells. The higher your blood sugar levels, the more hemoglobin you'll have with sugar attached. An A1C level of 6.5 percent or higher on two separate tests indicates you have diabetes. A result between 5.7 and 6.4 percent is considered prediabetes, which indicates a high risk of developing diabetes. Normal levels are below 5.7 percent.
If, on the other hand, you are already starting to develop complications or your medication regimen has changed because your blood sugars are getting higher, remember that diabetes is a progressive disease—and sometimes these things just happen without any influence from your own actions. As you age, beta cells in the pancreas get tired and stop working. If you've had diabetes for 20 years and now need to start insulin, for example, it doesn't mean you've failed. It just means that your body needs some help. Make sure you continue to receive education and that you continue to have someone to lean on when you need it, and keep the lines of communication open with your doctor. It truly can make a difference.

The typical symptoms of diabetes mellitus are the three “polys:” polyuria, polydipsia, and polyphagia. Because of insulin deficiency, the assimilation and storage of glucose in muscle adipose tissues, and the liver is greatly diminished. This produces an accumulation of glucose in the blood and creates an increase in its osmolarity. In response to this increased osmotic pressure there is depletion of intracellular water and osmotic diuresis. The water loss creates intense thirst and increased urination. The increased appetite (polyphagia) is not as clearly understood. It may be the result of the body's effort to increase its supply of energy foods even though eating more carbohydrates in the absence of sufficient insulin does not meet the energy needs of the cells.
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Is type 2 diabetes serious? Type 2 diabetes is not a death sentence, but it is a very serious disease that demands attention and careful monitoring. There is no such thing as ‘mild’ diabetes. Elevated glucose levels can damage the nervous system, blood vessels, eyes, heart, and kidneys. These complications really impact quality of life (through blindness, amputations, dialysis etc). They also significantly increase the chance of a stroke or heart attack. Managing blood glucose levels immediately, along with other health risk factors (e.g., cholesterol, blood pressure, weight), is necessary for preventing these complications. Losing even a small amount of weight and keeping it off can also improve glucose control as well as have other clinical benefits (read more tips on managing diet and exercise below for more on weight loss). Keep in mind that better diabetes management also has benefits in the here and now – mood and energy levels are adversely affected when your glucose levels are high. 
Patients with Type I diabetes need daily injections of insulin to help their bodies use glucose. The amount and type of insulin required depends on the height, weight, age, food intake, and activity level of the individual diabetic patient. Some patients with Type II diabetes may need to use insulin injections if their diabetes cannot be controlled with diet, exercise, and oral medication. Injections are given subcutaneously, that is, just under the skin, using a small needle and syringe. Injection sites can be anywhere on the body where there is looser skin, including the upper arm, abdomen, or upper thigh.
Rates of type 2 diabetes have increased markedly since 1960 in parallel with obesity.[17] As of 2015 there were approximately 392 million people diagnosed with the disease compared to around 30 million in 1985.[11][18] Typically it begins in middle or older age,[6] although rates of type 2 diabetes are increasing in young people.[19][20] Type 2 diabetes is associated with a ten-year-shorter life expectancy.[10] Diabetes was one of the first diseases described.[21] The importance of insulin in the disease was determined in the 1920s.[22]
Damage to small blood vessels can affect the eyes, kidneys, and nerves. Damage to eyes, specifically the retina, is called diabetic retinopathy and is the leading cause of blindness. Damage to the kidneys, called diabetic nephropathy, can lead to kidney failure and the need for dialysis. Damage to the nerves that supply the legs and arms and gastrointestinal tract is called diabetic neuropathy. Some people with diabetes who develop peripheral neuropathy (damage to the nerves in the legs) and have poor blood flow to the legs may eventually need an amputation.
Apart from severe DKA or hypoglycemia, type 1 diabetes mellitus has little immediate morbidity. The risk of complications relates to diabetic control. With good management, patients can expect to lead full, normal, and healthy lives. Nevertheless, the average life expectancy of a child diagnosed with type 1 diabetes mellitus has been variously suggested to be reduced by 13-19 years, compared with their nondiabetic peers. [34]
It is also important to note that currently one third of those who have IGT are in the productive age between 20-39 yr and, therefore, are likely to spend many years at high risk of developing diabetes and/or complications of diabetes1. Some persons with prediabetes experience reactive hypoglycaemia 2-3 hours after a meal. This is a sign of impaired insulin metabolism indicative of impending occurrence of diabetes. Therefore, periodic medical check-up in people with such signs or risk factors for diabetes would reduce the hazards involved in having undiagnosed diabetes. It would help improve the health status of a large number of people who otherwise would be silent sufferers from the metabolic aberrations associated with diabetes.
Type 2 diabetes was also previously referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult-onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells).
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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.
Part of a treatment plan for diabetes will involve learning about diabetes, how to manage it, and how to prevent complications. Your doctor, diabetes educator, or other health care professional will help you learn what you need to know so you are able to manage your diabetes as effectively as possible. Keep in mind that learning about diabetes and its treatment will take time. Involving family members or other people who are significant in your life can also help you manage your diabetes.
Most pediatric patients with diabetes have type 1 diabetes mellitus (T1DM) and a lifetime dependence on exogenous insulin. Diabetes mellitus (DM) is a chronic metabolic disorder caused by an absolute or relative deficiency of insulin, an anabolic hormone. Insulin is produced by the beta cells of the islets of Langerhans located in the pancreas, and the absence, destruction, or other loss of these cells results in type 1 diabetes (insulin-dependent diabetes mellitus [IDDM]). A possible mechanism for the development of type 1 diabetes is shown in the image below. (See Etiology.)

Insulin is a hormone produced by the beta cells within the pancreas in response to the intake of food. The role of insulin is to lower blood sugar (glucose) levels by allowing cells in the muscle, liver and fat to take up sugar from the bloodstream that has been absorbed from food, and store it away as energy. In type 1 diabetes (previously called insulin-dependent diabetes mellitus), the insulin-producing cells are destroyed and the body is not able to produce insulin naturally. This means that sugar is not stored away but is constantly released from energy stores giving rise to high sugar levels in the blood. This in turn causes dehydration and thirst (because the high glucose ‘spills over’ into the urine and pulls water out of the body at the same time). To exacerbate the problem, because the body is not making insulin it ‘thinks’ that it is starving so does everything it can to release even more stores of energy into the bloodstream. So, if left untreated, patients become increasingly unwell, lose weight, and develop a condition called diabetic ketoacidosis, which is due to the excessive release of acidic energy stores and causes severe changes to how energy is used and stored in the body.


Good metabolic control can delay the onset and progression of diabetic retinopathy. Loss of vision and blindness in persons with diabetes can be prevented by early detection and treatment of vision-threatening retinopathy: regular eye examinations and timely intervention with laser treatment, or through surgery in cases of advanced retinopathy. There is evidence that, even in developed countries, a large proportion of those in need is not receiving such care due to lack of public and professional awareness, as well as an absence of treatment facilities. In developing countries, in many of which diabetes is now common, such care is inaccessible to the majority of the population.
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.
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