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Effect of Acute Hyperglycemia on Insulin Secretion in Humans

¹ Metabolism Unit, CNR Institute of Clinical Physiology, and the Department of Internal Medicine, University of Pisa, Pisa, Italy
² CNR Institute of Systems Science and Biomedical Engineering, Padova, Italy

First-phase insulin response to intravenous glucose is impaired both in type 2 diabetic patients and in subjects at risk for the disease. Hyperglycemia can modify ß-cell response by either inhibiting or potentiating both first- and second-phase insulin release. In normal subjects, the effect of acute hyperglycemia on insulin secretion is controversial. We measured (in 13 healthy volunteers) insulin secretion (by deconvolution of plasma C-peptide concentrations) during three consecutive 30-min hyperglycemic steps (2.8, 2.8, and 5.6 mmol/l), followed by an intravenous arginine bolus. First-phase insulin secretion in response to the first hyperglycemic step (456 ± 83 pmol · min^-1 · m^-2) was significantly larger than that in response to the second step (311 ± 37 pmol · min^-1 · m^-2, P < 0.01); the subsequent increase in glycemia failed to stimulate first-phase secretion any further (377 ± 60 pmol · min^-1 · m^-2, NS vs. the previous value). This inhibition was also evident when insulin release rates were corrected for the respective increments (absolute or percentage) in plasma glucose levels and was not due to ß-cell exhaustion because the arginine bolus still elicited a large peak of insulin secretion (4,790 ± 2,330 pmol · min^-1 · m^-2). In contrast, second-phase insulin secretion was related to the prevailing glucose levels across the three hyperglycemic steps in a direct quasilinear manner. We conclude that first-phase insulin secretion is inhibited by short-term modest hyperglycemia, whereas the second-phase insulin secretion increases linearly with hyperglycemia.

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