Traditionally, physicians have categorized diabetes mellitus (DM) as Type I (formerly called insulin dependent or juvenile onset), Type II (formerly called non-insulin dependent or adult onset), and gestational diabetes. Because the pathogenesis and risk factors differ for each form of DM, each are considered separately.
Type I DM accounts for approximately 10% of diabetes cases, and most cases come to medical attention by adolescence. This form of diabetes results from the destruction of the insulin producing beta cells found in the islets of Langerhans that make up the endocrine pancreas. The destruction is mediated by the immune system; as such, Type I DM is considered an autoimmune disease. When 90% of the beta cells are destroyed, the person develops the classic symptoms of insulin deficiency: weight loss, fatigue, excessive thirst (polydypsia), excessive hunger (polyphagia), and excessive urine output (polyuria).
Although cases of Type I DM have been described since ancient times, the risk factors for this disease remain largely unknown. Some speculate that exposure to certain viruses during childhood provokes an autoimmune reaction, leading to destruction of the islet cells. Some scientists consider people with the HLA protein DQ3.1 to be at higher risk for Type I DM. Neither theory seems to carry much weight however, as no specific infectious agent has been linked to the disease, and most people with the DQ3.1 haplotype never develop Type I DM. As far as genetic predisposition or vulnerability go, most cases of Type I DM occur sporadically. Although a positive family history should not be discounted altogether, no clear pattern of heredity seems to exist for this form of diabetes.
Type II DM accounts for nearly 90% of cases of diabetes in the US and industrialized world.In contrast to Type I DM, Type II DM has a clear cut set of risk factors: a positive family history and obesity. Although the incidence of Type II DM is increasing in nearly all groups of people, Native Americans seem to be the hardest hit, followed by African Americans, Latinos, Asians, and Caucasians.
Type II DM is believed to result from a person’s liver, skeletal muscles, and fat tissue becoming progressively unresponsive to the actions of insulin. In medical jargon this is known as end organ insensitivity or insulin resistance. Although Type II DM can often be controlled with diet, exercise, and oral hypoglycemic medications (metformin, glipizide), 25% or more of people with the disease will eventually require insulin injections to control their blood sugar levels. Type II DM seldom strikes before age 40; however, clinicians have reported cases of in increasingly younger patients, especially in morbidly obese adolescents.
The third category of DM, gestational diabetes, occurs in pregnant women. Although a positive family history and obesity probably raise the risk of gestational DM, most women who develop this condition have no obvious risk factors. According to one theory, most pregnant women develop insulin resistance to some degree, owing to the effects of a host of elevated hormones including hCG, hCS, and estrogen. Most pregnant women are given an oral glucose tolerance test to screen for gestational diabetes. Gestational DM is managed with insulin injections. Gestational DM usually resolves after delivery, but a significant percentage of these women develop insulin dependent diabetes 10 or more years later.