Pancreatic alpha- and beta-cell responses to GIP infusion in normal man.

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Abstract
Evidence is increasing that the major gut hormone responsible for augmentation of insulin secretion is gastric inhibitory polypeptide (GIP). Further understanding of the role of GIP on the function of .alpha.- and .beta.-cells of the pancreas and the dependence of this interaction on the ambient glucose concentration can be gained from the application of the glucose-clamp technique. Highly purified porcine GIP was administered i.v. at a dose of 6.7 ng/(kg .cntdot. min) for 90 min under the following conditions: (A), during basal-state euglycemia; (B), after the establishment of mild, steady-state hyperglycemia at a plasma glucose level 54 mg/dl above basal; and (C), after the establishment of moderate, steady-state hyperglycemia at a plasma glucose level of 143 mg/dl above basal. In all 3 conditions, plasma GIP levels were within the physiological range. Under condition A, no changes in plasma immunoreactive insulin (IRI), immunoreactive glucagon (IRG) or glucose were observed. Under condition B, IRG was suppressed by the hyperglycemia and no further effect was observed during or after the GIP infusion. IRI levels were modestly augmented. Under condition C, IRG responded as in condition B. IRI levels in condition C were markedly elevated by GIP infusion. Biological half-life of GIP ranged from 13-26 min under the conditions of these studies. GIP, whether endogenously released or exogenously administered in physiological concentrations, is apparently a gastrointestinal mediator of insulin release; its effect is dependent on the ambient blood glucose level. GIP is probably not glucagonotropic in normal man during euglycemic or hyperglycemic conditions.