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