Reduced secretion of gastric inhibitory polypeptide in Turner patients with impaired glucose tolerance.

There is a well documented increase in the incidence of abnormal glucose tolerance in patients with Turner syndrome. To elucidate the pathophysiology of this phenomenon, we studied the serum concentrations of gastric inhibitory polypeptide (GIP)--as probably the most important hormonal factor of the entero-insular axis--in relation to impaired glucose tolerance in this syndrome. Oral glucose tolerance tests were performed in 12 Turner patients with simultaneous determination of plasma glucose, insulin and GIP. An impaired glucose tolerance (iGT) was found in four patients with a chronological age between 12.3 and 14.9 years. These patients were compared with four Turner patients of similar age and weight and a normal glucose tolerance (nGT). The highest insulin level occurred 90 min after stimulation in the patients with iGT compared to 30 min in the nGT group. Interestingly, the total areas under the insulin curves were not different. Stimulated plasma GIP concentrations and the areas under the GIP curves were significantly lower in iGT compared to nGT patients. A disturbed entero-insular axis might contribute to the delayed--rather than diminished--release of insulin in patients with Turner syndrome and impaired glucose tolerance.