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.
Diabetic foot disease, due to changes in blood vessels and nerves, often leads to ulceration and subsequent limb amputation. It is one of the most costly complications of diabetes, especially in communities with inadequate footwear. It results from both vascular and neurological disease processes. Diabetes is the most common cause of non-traumatic amputation of the lower limb, which may be prevented by regular inspection and good care of the foot.

Type 2 diabetes usually begins with insulin resistance, a condition in which muscle, liver, and fat cells do not use insulin well. As a result, your body needs more insulin to help glucose enter cells. At first, the pancreas makes more insulin to keep up with the added demand. Over time, the pancreas can’t make enough insulin, and blood glucose levels rise.

Because both yeast and bacteria multiply more quickly when blood sugar levels are elevated, women with diabetes are overall at a higher risk of feminine health issues, such as bacterial infections, yeast infections, and vaginal thrush, especially when blood sugar isn't well controlled. And a lack of awareness about having prediabetes or diabetes can make managing blood sugar impossible.

While it's conceivable that scientists will isolate a single factor as causing type 1 and type 2, the much more likely outcome is that there is more than one cause. Each person seems to take a unique path in developing diabetes. Someday, doctors may be able to assess an individual's genetic risk for diabetes, allowing him or her to dodge the particular environmental factors that would trigger the disease. And perhaps if the baffling question of why a person gets diabetes can be put to rest, the answer will also offer a cure for the disease.


Supporting evidence for Shulman's theory comes from observations about a rare genetic illness called lipodystrophy. People with lipodystrophy can't make fat tissue, which is where fat should properly be stored. These thin people also develop severe insulin resistance and type 2 diabetes. "They have fat stored in places it doesn't belong," like the liver and muscles, says Shulman. "When we treat them . . . we melt the fat away, reversing insulin resistance and type 2 diabetes." Shulman's theory also suggests why some people who carry extra fat don't get type 2. "There are some individuals who store fat [under the skin] who have relatively normal insulin sensitivity, a so-called fit fat individual," he says. Because of the way their bodies store fat, he believes, they don't get diabetes.
When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption, and glucose will be excreted in the urine (glycosuria).[62] 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 will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[60]
^ Jump up to: a b 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. PMID 19726018.
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.[61]
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.[74]
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.)
John P. Cunha, DO, is a U.S. board-certified Emergency Medicine Physician. Dr. Cunha's educational background includes a BS in Biology from Rutgers, the State University of New Jersey, and a DO from the Kansas City University of Medicine and Biosciences in Kansas City, MO. He completed residency training in Emergency Medicine at Newark Beth Israel Medical Center in Newark, New Jersey.

Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400–500 AD with type 1 associated with youth and type 2 with being overweight.[110] 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.[110] Effective treatment was not developed until the early part of the 20th century when the Canadians Frederick Banting and Charles Best discovered insulin in 1921 and 1922.[110] This was followed by the development of the long acting NPH insulin in the 1940s.[110]
In an otherwise healthy individual, blood glucose levels usually do not rise above 180 mg/dL (9 mmol/L). In a child with diabetes, blood sugar levels rise if insulin is insufficient for a given glucose load. The renal threshold for glucose reabsorption is exceeded when blood glucose levels exceed 180 mg/dL (10 mmol/L), causing glycosuria with the typical symptoms of polyuria and polydipsia. (See Pathophysiology, Clinical, and Treatment.)
Pre-clinical diabetes refers to the time during which destruction of pancreatic insulin-producing cells is occurring, but symptoms have not yet developed. This period may last for months to years. Normally, 80-90% of the pancreatic beta cells must be destroyed before any symptoms of diabetes develops. During this time, blood tests can identify some immunological markers of pancreatic cell destruction. However, there is currently no known treatment to prevent progression of pre-clinical diabetes to true diabetes mellitus.
Type 1 diabetes mellitus has wide geographic variation in incidence and prevalence. [30] Annual incidence varies from 0.61 cases per 100,000 population in China to 41.4 cases per 100,000 population in Finland. Substantial variations are observed between nearby countries with differing lifestyles, such as Estonia and Finland, and between genetically similar populations, such as those in Iceland and Norway.
Jump up ^ Haw JS, Galaviz KI, Straus AN, Kowalski AJ, Magee MJ, Weber MB, Wei J, Narayan KM, Ali MK (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.
Patients need to ensure that their blood glucose levels are kept as normal as possible so that delicate tissues in the body (especially blood vessels in the eyes, kidneys and peripheral nerves) are not damaged by high glucose levels over a long period of time. To achieve this, patients need to measure their glucose regularly and learn how to adjust their insulin doses in order to optimise their glucose levels (diabetes control). Good diabetes control helps to minimise the risk of long-term diabetes complications, as well as short-term symptoms (such as thirst).

Jump up ^ Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, Ingelsson E, Lawlor DA, Selvin E, Stampfer M, Stehouwer CD, Lewington S, Pennells L, Thompson A, Sattar N, White IR, Ray KK, Danesh J (June 2010). "Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies". Lancet. 375 (9733): 2215–22. doi:10.1016/S0140-6736(10)60484-9. PMC 2904878. PMID 20609967.
Doctors may recommend one or more types of medications to help control diabetes. While taking medications, it's important for people with diabetes to regularly test their blood glucose levels at home. There are many different blood glucose meters available on the market. Speak to a doctor or pharmacist about these meters to help you select the best meter for your needs.
It is clearly established that diabetes mellitus is not a single disease but a genetically heterogeneous group of disorders that share glucose intolerance in common (4–7). The concept of genetic heterogeneity (i.e. that different genetic and/or environmental etiologic factors can result in similar phenotypes) has significantly altered the genetic analysis of this common disorder. Diabetes and glucose intolerance are not diagnostic terms, but, like anemia, simply describe symptoms and/or laboratory abnormalities that can have a number of distinct etiologies.
Oral Agents. Oral antidiabetic drugs (see hypoglycemic agents) are sometimes prescribed for patients with type 2 diabetes who cannot control their blood glucose with diet and exercise. These are not oral forms of insulin; they are sulfonylureas, chemically related to the sulfonamide antibiotics. Patients receiving them should be taught that the drug they are taking does not eliminate the need for a diet and exercise program. Only the prescribed dosage should be taken; it should never be increased to make up for dietary indiscretions or discontinued unless authorized by the physician.
All children with type 1 diabetes mellitus require insulin therapy. Most require 2 or more injections of insulin daily, with doses adjusted on the basis of self-monitoring of blood glucose levels. Insulin replacement is accomplished by giving a basal insulin and a preprandial (premeal) insulin. The basal insulin is either long-acting (glargine or detemir) or intermediate-acting (NPH). The preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-acting (regular).
interventions The goal of treatment is to maintain insulin glucose homeostasis. Type 1 diabetes is controlled by insulin, meal planning, and exercise. The Diabetes Control and Complications Trial (DCCT), completed in mid-1993, demonstrated that tight control of blood glucose levels (i.e., frequent monitoring and maintenance at as close to normal as possible to the level of nondiabetics) significantly reduces complications such as eye disease, kidney disease, and nerve damage. Type 2 diabetes is controlled by meal planning; exercise; one or more oral agents, in combination with oral agents; and insulin. The results of the United Kingdom Prospective Diabetes Study, which involved more than 5000 people with newly diagnosed type 2 diabetes in the United Kingdom, were comparable to those of the DCCT where a relationship in microvascular complications. Stress of any kind may require medication adjustment in both type 1 and type 2 diabetes.
2.Retinopathy - Diabetes may cause blood vessels in the retina (the light sensitive lining of the eye) to become leaky, blocked, or grow abnormally [Figure 1]. Retinopathy is rare before the age of 10 and the risk increases with the length of time a person has diabetes. Treatments such as laser, injections in the eye, or other procedures may be helpful to prevent visual loss or restore sight. The longer a patient has diabetes, the greater chance of developing an eye problem.  All patients with diabetes are at risk for developing retinopathy, but the risk is higher for patients with worse blood sugar control.  Early retinopathy may have no symptoms, but early treatment is essential to prevent any loss of vision.
We use cookies and similar technologies to improve your browsing experience, personalize content and offers, show targeted ads, analyze traffic, and better understand you. We may share your information with third-party partners for marketing purposes. To learn more and make choices about data use, visit our Advertising Policy and Privacy Policy. By clicking “Accept and Continue” below, (1) you consent to these activities unless and until you withdraw your consent using our rights request form, and (2) you consent to allow your data to be transferred, processed, and stored in the United States.
×