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SUNY-Downstate Medical Center, 450 Clarkson Ave., Box 1205, Brooklyn, NY 11203. Fax 718-447-1558; e-mail hlebovitz{at}IBM.net
Type 2 diabetes is a heterogeneous disorder. Clinical expression of the
disorder requires both genetic and environmental factors. One theory
concerning its etiology is that it is the result of the evolution of a
thrifty genotype that had survival benefits in the past but is
detrimental in the current environment. An opposing theory is that it
represents an adult metabolic response to fetal malnutrition.
Hyperglycemia in type 2 diabetes results from absolute or relative
insulin deficiency. Most often relative insulin deficiency is
attributable to an inability to adequately compensate for insulin
resistance. Insulin resistance may be caused by a variety of genetic or
metabolic factors. The most common etiological factor in insulin
resistance is central obesity. Insulin resistance is associated with a
cluster of metabolic abnormalities that include glucose intolerance,
hypertension, a unique dyslipidemia, a procoagulant state, and an
increase in macrovascular disease. Clinical intervention studies have
demonstrated that reduction in the chronic microvascular and
macrovascular complications of type 2 diabetes requires treatment of
hyperglycemia to achieve hemoglobin A1c <7.0%, blood pressure
130/80 mmHg, and plasma LDL-cholesterol
2.6 mmol/L (
100 mg/dL).
Oral antihyperglycemic agents increase endogenous insulin secretion,
decrease insulin resistance, or lower postprandial plasma glucose rise
by delaying absorption of complex carbohydrates. Long-term glycemic
control in type 2 diabetes requires progressive, stepwise, combination
treatment with oral agents and eventually combination treatment with
oral agents and insulin.© 1999 American Association for
Clinical Chemistry
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