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Diabetes, Vol 38, Issue 12 1501-1505, Copyright © 1989 by American Diabetes Association


ARTICLES

Type II diabetes, glucose "non-sense," and islet desensitization

RP Robertson
Diabetes Center, University of Minnesota, Minneapolis 55455.

A universal finding in hyperglycemic patients with type II (non-insulin-dependent) diabetes mellitus is that all share a common defect in glucose recognition resulting in abnormal insulin secretion by pancreatic islet beta-cells. This defect is 1) specific for glucose signals rather than global, 2) related to chronic hyperglycemia, and 3) partially reversible after brief treatment with insulin to induce normoglycemia and through use of other pharmacological agents without normalizing glucose levels. My perspective is that an essential component of this defect is secondary and may represent a state of homologous desensitization of the beta-cell secretory apparatus to glucose. Elucidation of the biochemical mechanism(s) of defective recognition of glucose signals by beta-cells--or glucose "non-sense"--in these patients will provide key insights into the pathogenesis of type II diabetes mellitus.
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