TYPE 1 DIABETES
Type 1 diabetes is characterized by destruction of the pancreatic beta cells. It is thought that combined genetic, immunologic, and possibly environmental (eg, viral) factors contribute to beta cell destruction. Although the events that lead to beta cell de-struction are not fully understood, it is generally accepted that a genetic susceptibility is a common underlying factor in the de-velopment of type 1 diabetes. People do not inherit type 1 dia-betes itself; rather, they inherit a genetic predisposition, or tendency, toward developing type 1 diabetes. This genetic ten-dency has been found in people with certain HLA (human leukocyte antigen) types. HLA refers to a cluster of genes responsible for transplantation antigens and other immune processes. About 95% of Caucasians with type 1 diabetes exhibit specific HLA types (DR3 or DR4). The risk of developing type 1 diabetes is increased three to five times in people who have one of these two HLA types. The risk increases 10 to 20 times in peo-ple who have both DR3 and DR4 HLA types (as compared with the general population). Immune-mediated diabetes commonly develops during childhood and adolescence, but it can occur at any age (ADA, Expert Committee on the Diagnosis and Classi-fication of Diabetes Mellitus, 2003).
There is also evidence of an autoimmune response in type 1 diabetes. This is an abnormal response in which antibodies are di-rected against normal tissues of the body, responding to these tis-sues as if they are foreign. Autoantibodies against islet cells and against endogenous (internal) insulin have been detected in people at the time of diagnosis and even several years before the development of clinical signs of type 1 diabetes. In addition to genetic and immunologic components, environmental factors, such as viruses or toxins, that may initiate destruction of the beta cell are being investigated.
Regardless of the specific etiology, the destruction of the beta cells results in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. In addition, glucose derived from food cannot be stored in the liver but in-stead remains in the bloodstream and contributes to postprandial (after meals) hyperglycemia. If the concentration of glucose in the blood exceeds the renal threshold for glucose, usually 180 to 200 mg/dL (9.9 to 11.1 mmol/L), the kidneys may not reabsorb all of the filtered glucose; the glucose then appears in the urine (glucosuria). When excess glucose is excreted in the urine, it is ac-companied by excessive loss of fluids and electrolytes. This is called osmotic diuresis.
Because insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenesis (production of new glu-cose from amino acids and other substrates), in people with in-sulin deficiency, these processes occur in an unrestrained fashion and contribute further to hyperglycemia. In addition, fat break-down occurs, resulting in an increased production of ketone bodies, which are the byproducts of fat breakdown.
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