THE ETIOLOGY OF DIABETES MELLITUS Written by Wong Hon Long
Diabetes mellitus is a chronic disease characterized by relative or absolute deficiency of insulin, resulting in glucose intolerance. It occurs in 4-5 million persons in United States (approximately 2% of population). The classic symptoms of diabetes mellitus result from abnormal glucose metabolism. The lack of insulin activity results in failure of transfer of glucose from plasma into cells. This situation so called “starvation in midst of plenty”. The body responds as if it were in fasting state, with stimulation of glucogenolysis, gluconeogenesis and lipolysis producing ketone bodies.The glucose absorbed during a meal is not metabolized at normal rate and therefore accumulates in blood (hyperglycemia) to be excreted in urine (glycosuria). Glucose in urine causes osmotic diuresis, leading to increase urine production (polyuria). Stimulation of protein breakdown to provide amino acids for gluconeogenesis results in muscle wasting and weight loss. These classic symptoms occur only in patients with severe insulin deficiency, most commonly in type I diabetes. Many patients with type II diabetes do not have these symptoms and present with one of complications of diabetes. Generally, there are two types of diabetes: Type I Diabetes Mellitus (insulin- dependent diabetes mellitus, IDDM) and Type II Diabetes Mellitus (non-insulin- dependent diabetes mellitus, NIDDM). Type I Diabetes Mellitus (insulin- dependent diabetes mellitus, IDDM) is due to destruction of pancreatic B cells. The cause of B cell destruction in type I diabetes is unknown. A few cases have followed viral infections, most commonly with coxsakievirus B or mumps virus. Autoimmunity is believed to be major mechanism involved. Islet cell autoantibodies are present in serum of 90% of newly diagnosed cases. Such antibodies are directed against several cell components, including cytoplasmic and membrane antigens or against insulin itself (IgG and IgE antibodies). Sensitized T lymphocytes with activity against B cells have also been demonstrated in some patients. Plasma insulin levels are very low or even absent in type I diabetes, and ketoacidosis develops if patients do not receive exogenous insulin. Type I diabetes occurs most commonly in juveniles, with highest incidence worldwide among 10- to 14-year-old group, but occasionally occurs in adults, especially nonobese and those who are elderly when hyperglycemia first appears.
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