Type 2 diabetes: An overview

Type 2 diabetes is a heterogeneous disorder. Clinical expression of the dis order requires both genetic and environmental factors. One theory concernin g its etiology is that it is the result of the evolution of a thrifty genot ype that had survival benefits in the past but is detrimental in the curren t environment. An opposing theory is that it represents an adult metabolic response to fetal malnutrition. Hyperglycemia in type 2 diabetes results fr om absolute or relative insulin deficiency. Most often relative insulin def iciency is attributable to an inability to adequately compensate for insuli n resistance. Insulin resistance may be caused by a variety of genetic or m etabolic factors. The most common etiological factor in insulin resistance is central obesity. Insulin resistance is associated with a cluster of meta bolic abnormalities that include glucose intolerance, hypertension, a uniqu e dyslipidemia, a procoagulant state, and an increase in macrovascular dise ase. Clinical intervention studies have demonstrated that reduction in the chronic microvascular and macrovascular complications of type 2 diabetes re quires treatment of hyperglycemia to achieve hemoglobin Ale <7.0%, blood pr essure less than or equal to 130/80 mmHg, and plasma LDL-cholesterol less t han or equal to 2.6 mmol/L (less than or equal to 100 mg/dL). Oral antihype rglycemic agents increase endogenous insulin secretion, decrease insulin re sistance, or lower postprandial plasma glucose rise by delaying absorption of complex carbohydrates. Longterm glycemic control in type 2 diabetes requ ires progressive, stepwise, combination treatment with oral agents and even tually combination treatment with oral agents and insulin. (C) 1999 America n Association for Clinical Chemistry.