Stimulation by Gastric Inhibitory Polypeptide of Insulin and Glucagon Secretion by Rat Islet Cultures

Abstract
Physiologic amounts of GIP [gastric inhibitory polypeptide] stimulated the secretion of IRI [immunoreactive insulin] and IRG [immunoreactive glucagon] by monolayer cultures of neonatal rat pancreatic islets. Localization of exogenous GIP to a minority subpopulation of the islet cells was observed. The results may be interpreted to indicate that the effect of GIP or IRI release by the B cell is not direct, but rather, is mediated through its action on another islet cell type. Conversely, the action of GIP on IRG release may be directly mediated through an effect of GIP on the A cell. The action of GIP on IRG release apparently overrides any suppressive effect that high glucose levels may exert. The stimulation by GIP of both IRI and IRG release was greater when a mixture of amino acids was omitted.