Effect of GIP on insulin release to intravenous glucose infusion in hyperthyroid rats.
Triiodothyronine induced hyperthyroidism caused significantly elevated basal and stimulated glucose and insulin levels in rats. The release of Gastric Inhibitory Polypeptide (GIP) following an oral glucose load was not significantly different between euthyroid and hyperthyroid rats. The insulin response, however, was significantly higher in hyperthyroid rats. Following intravenous glucose hyperthyroid rats showed a diminished insulin response when compared with euthyroid rats but intravenous infusion of glucose together with GIP caused a significantly higher insulin response in hyperthyroid rats. It is hypothesized that in hyperthyroidism there is an increased sensitivity to the insulinotropic action of GIP and that this mechanism could emphasize the importance of the enteroinsular axis in pathophysiological states.
D000284:Administration, Oral; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004195:Disease Models, Animal; D005749:Gastric Inhibitory Polypeptide / Q000494:pharmacology*; D005947:Glucose / Q000008:administration & dosage / Q000494:pharmacology*; D006980:Hyperthyroidism / Q000139:chemically induced / Q000503:physiopathology*; D007263:Infusions, Parenteral; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014284:Triiodothyronine
D001786:Blood Glucose; D007328:Insulin; D014284:Triiodothyronine; D005749:Gastric Inhibitory Polypeptide; D005947:Glucose