Glucose-Stimulated Insulin Secretion in Gastric Bypass Patients with Hypoglycemic Syndrome: No Evidence for Inappropriate Pancreatic β-cell Function
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- Kim, S.H., Abbasi, F., Lamendola, C. et al. OBES SURG (2010) 20: 1110. doi:10.1007/s11695-010-0183-2
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.
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).
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).
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.