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- Title
Mechanisms for Hyperglycemia in the Metabolic Syndrome: The Key Role of β-Cell Dysfunction.
- Authors
PORTE, DANIEL
- Abstract
ABSTRACT: Hyperglycemia in Type 2 diabetes represents a steady-state re-regulation of plasma glucose to a higher-than-normal level after an overnight fast. The underlying pathophysiology represents an interaction between impaired β-cell function and peripheral and hepatic insulin resistance which leads to abnormal hepatic glucose production. Subjects with the Metabolic Syndrome are at an increased risk for Type 2 diabetes and often have one or both of these disorders present even when glucose tolerance is normal. Thus, sophisticated measures of β-cell function and insulin sensitivity demonstrate a high frequency in populations characterized as having a high prevalence of atherosclerosis, central obesity, hypertension, and dyslipidemia with or without impaired glucose tolerance. Hyperglycemia compensates for the impairment of β-cell function and therefore, in our view, the β-cell is the critical factor in its development. Hyperinsulinemia, a curvilinear compensation for insulin resistance that is closely correlated with central adiposity, is another important predictor of hyperglycemia. In a Japanese-American population followed for five years, impaired β-cell function was present at baseline and preceded the accumulation of intraabdominal fat in those who developed Type 2 diabetes five years later. This interaction between these two pathophysiologic abnormalities in this sequence supports the hypothesis that β-cell dysfunction contributes to the development of central adiposity by reduced CNS insulin signaling.
- Publication
Annals of the New York Academy of Sciences, 1999, Vol 892, Issue 1, p73
- ISSN
0077-8923
- Publication type
Article
- DOI
10.1111/j.1749-6632.1999.tb07786.x