Hypersecretion of gastric inhibitory polypeptide in nondiabetic children with cystic fibrosis.
Failure of secretion of an insulinotropic enteric hormone has been postulated as a cause for the impaired insulin secretion observed following a glycemic stimulus in children with cystic fibrosis (CF). Gastric inhibitory polypeptide (GIP), a hormone located primarily in the duodenum, is the main hormonal stimulus to insulin release from the gastrointestinal tract. To determine whether hyposecretion of GIP was present in CF subjects, GIP secretion was measured in 15 control children and ten children with CF, following a standard oral glucose tolerance test. None of the subjects was diabetic but the CF children demonstrated significant insulinopenia compared to the normal control subjects. GIP secretion in the CF children was significantly greater than in the normal control subjects (normal, 38.8 +/- 4.6 ng/ml . min; CF, 54.9 +/- 6.1 ng/ml . min, P less than .01). These findings indicate that there is increased production of GIP in CF children rather than impaired secretion as had been postulated. The demonstration of hypersecretion of GIP in nondiabetic insulinopenic individuals adds further support to the hypothesis that insulin exerts feedback control on GIP secretion.