Role of gastric inhibitory polypeptide in postprandial hyperinsulinemia of obesity

L. R. Roust, M. Stesin, V. L.W. Go, P. C. O'Brien, R. A. Rizza, F. J. Service

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


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 < 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.

Original languageEnglish (US)
Pages (from-to)17/6
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Issue number6
StatePublished - Jan 1 1988

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)


Dive into the research topics of 'Role of gastric inhibitory polypeptide in postprandial hyperinsulinemia of obesity'. Together they form a unique fingerprint.

Cite this