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.
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