AJP - Endocrinology and Metabolism, Vol 254, Issue 6 E767-E774, Copyright © 1988 by American Physiological Society
Role of gastric inhibitory polypeptide in postprandial hyperinsulinemia of obesity
L. R. Roust, M. Stesin, V. L. Go, P. C. O'Brien, R. A. Rizza and F. J. Service
Department of Epidemiology and Statistics, Mayo Foundation, Rochester, Minnesota 55905.
To assess the contribution of gastric inhibitory polypeptide (GIP) to the
postprandial hyperinsulinemia of obesity, secretion rates of GIP (generated
from kinetic analyses from infusions of porcine GIP) and insulin (from
C-peptide applied to a validated kinetic model) to meals of 3 sizes were
determined in 10 obese (5 male and 5 female) and 10 lean, sex- and
age-matched healthy subjects. Although the postprandial secretion rates of
GIP were greater in obese subjects (P = 0.03), postprandial concentrations
of GIP were not. The latter may be explained by the greater volume of
distribution of GIP in obese subjects (P = 0.036). Secretion rates and
volume of distribution of GIP were correlated (r = 0.652, P less than
0.01). Despite excessive integrated postprandial (P = 0.010) insulin
concentrations, insulin secretion was not significantly different between
obese and lean subjects. We conclude that 1) although postprandial plasma
GIP concentrations are normal, GIP secretion is increased in obesity, 2)
the postprandial hyperinsulinemia of obesity is not due to excessive
insulin secretion but is likely secondary to altered insulin clearance, and
3) GIP cannot account for the hyperinsulinemia of obesity through its
insulinotropic action.
