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Obes Surg. 2010 Aug;20(8):1110-6. doi: 10.1007/s11695-010-0183-2.

Glucose-stimulated insulin secretion in gastric bypass patients with hypoglycemic syndrome: no evidence for inappropriate pancreatic beta-cell function.

Author information

1
Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA. sunhkim@stanford.edu

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 beta-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 <or= 0.046) and insulin-resistant groups (p <or= 0.001). Pancreatic beta-cell sensitivity to glucose (slope relating glucose and ISR) was lowest in the RYGB group (p <or= 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.

PMID:
20665189
DOI:
10.1007/s11695-010-0183-2
[Indexed for MEDLINE]

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