-
Views
-
Cite
Cite
Angeliki Hadji-Georgopoulos, Maria Ines Schmidt, Dariush Elahi, Richard Hershcopf, A. Avinoam Kowarski, Increased Gastric Inhibitory Polypeptide Levels in Patients with Symptomatic Postprandial Hypoglycemia, The Journal of Clinical Endocrinology & Metabolism, Volume 56, Issue 4, 1 April 1983, Pages 648–652, https://doi.org/10.1210/jcem-56-4-648
Close - Share Icon Share
In a previous study it was found that patients with syptomatic postprandial hypoglycemia (SPH) showed delayed hyperinsulinemia. To further investigate the mechanism of this delayed hyperinsulinemia, oral and iv glucose tolerance tests (GTTs) were performed at different times on each of 11 asymptomatic (control) and 13 SPH nonobese subjects. Blood glucose levels were monitored continuously, and plasma levels of immunoreactive insulin (IRI) were measured intermittently. After oral GTT, SPH patients showed a lower blood glucose nadir than asymptomatic controls [46 ± 5 mg/dl (mean ± SD), associated with symptoms, vs. 63 ± 10 mg/dl, respectively]. A delayed insulin peak was also observed in the SPH patients (at 108 ± 36 min vs. 60 ± 30 min in the controls). By contrast, after iv GTT, none of the SPH patients had symptoms, and none had a lower blood glucose nadir or a delayed insulin peak compared to controls.
In 11 SPH and 11 control subjects, plasma IRI and immunoreactive gastric inhibitory polypeptide (IR-GIP) were measured every 30 min up to 120 min after glucose ingestion. In all of the SPH and 4 of the control subjects, IRI and IR-GIP measurements were extended up to 300 min. Mean IR-GIP levels were significantly higher at zero time; 60, 90, and 120 min after glucose ingestion; and 30, 60, and 90 min before the glucose nadir (P < 0.05 to P < 0.005). Moreover, plasma IR-GIP and IRI levels 30 min before the glucose nadir correlated significantly with the subsequent rate of blood glucose fall (r = 0.562 and r = 0.834, respectively).
We conclude that a gastrointestinal factor(s) is necessary for the development of SPH, and that elevated and prolonged IRGIP levels could account for the delayed hyperinsulinemia observed in SPH patients after glucose ingestion. (J Clin Endocrinol Metab56: 648,1983)
