Erschienen in:
01.08.2010 | Clinical Research
Glucose-Stimulated Insulin Secretion in Gastric Bypass Patients with Hypoglycemic Syndrome: No Evidence for Inappropriate Pancreatic β-cell Function
verfasst von:
Sun H. Kim, Fahim Abbasi, Cindy Lamendola, Gerald M. Reaven, Tracey McLaughlin
Erschienen in:
Obesity Surgery
|
Ausgabe 8/2010
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Abstract
Background
Roux-en-Y gastric bypass surgery (RYGB) has been associated with a hypoglycemic syndrome characterized by postprandial hypoglycemia and hyperinsulinemia. The syndrome is believed to occur due to insulin hypersecretion from either pancreatic β-cell hyperplasia or hyperfunction.
Methods
Eight RYGB patients with hypoglycemic syndrome had insulin secretion rates determined during a 240-min graded intravenous glucose infusion. They were compared to 34 nondiabetic, nonsurgical individuals who were divided based on their insulin sensitivity status as measured by the insulin suppression test: insulin-sensitive (n = 8), insulin intermediate (n = 7), and insulin-resistant (n = 19).
Results
RYGB patients had insulin concentrations and HOMA-IR similar to the insulin-sensitive reference group. In addition, integrated insulin secretion rates were comparable to the insulin-sensitive group and significantly lower than the insulin intermediate (p ≤ 0.046) and insulin-resistant groups (p ≤ 0.001). Pancreatic β-cell sensitivity to glucose (slope relating glucose and ISR) was lowest in the RYGB group (p ≤ 0.04).
Conclusions
Patients with hypoglycemic syndrome post-RYGB do not have generalized hypersecretion of insulin and appear to have appropriate insulin secretion rate in response to intravenous glucose.