Open AccessPancreatic Islet Hormone Response to Oral Glucose in Morbidly Obese Patients
Author(s) -
Kenneth R. Sirinek,
Thomas M. O'Dorisio,
Brent Howe,
Arthur S. McFee
Publication year - 1985
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-198506000-00004
Subject(s) - medicine , morbidly obese , islet , endocrinology , hormone , insulin , obesity , weight loss
Pancreatic islet peptides, as well as other gastrointestinal hormones, have been implicated in both the pathogenesis of obesity and the etiology of associated metabolic derangements. This study evaluated the pancreatic islet and gastrointestinal (GI) hormone response to oral glucose in 20 morbidly obese (151% above ideal body weight) patients. Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Significant release of PP occurred in 14 patients, while only six patients had release of somatostatin. No significant changes in plasma concentrations of glucagon occurred. Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Failure of glucagon suppression in response to oral glucose many contribute to the hyperglycemia noted. Somatostatin and pancreatic polypeptide may be responsible for some of the metabolic derangements of morbid obesity.