Impact of Gastric Bypass Surgery on Gut Hormones and Glucose Homeostasis in Type 2 Diabetes

  1. Erik Näslund1 and
  2. John G. Kral2
  1. 1Division of Surgery, Karolinska Institutet Danderyd Hospital, Stockholm, Sweden
  2. 2Department of Surgery, State University of New York, Downstate Medical Center, Brooklyn, New York
  1. Address correspondence and reprint requests to Erik Näslund, MD, PhD, Division of Surgery, Karolinska Institutet, Danderyd Hospital, SE-182 88 Stockholm, Sweden. E-mail: erik.naslund{at}ki.se

Abstract

Gastric bypass surgery (GBP) for obesity, by constructing an isolated ∼30-ml proximal gastric pouch connected to a 75-cm limb of proximal jejunum, bypassing >90% of the stomach, the pylorus, and the duodenum, cures type 2 diabetes in >80% of cases. We review alterations in gastrointestinal peptide release after GBP that affect glucose disposal. We focus on ghrelin and the incretins glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, and peptide YY as the most likely candidates for increasing insulin sensitivity after these operations, even before substantial weight loss has occurred. Although we have limited our review to only four gastrointestinal peptides, others may be involved, as are adipocyte-derived molecules such as leptin and adiponectin, and substrate receptor interactions in target tissues including the brain.

Footnotes

  • This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educational grant from Servier.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted April 21, 2006.
    • Received March 26, 2006.
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