GLP-1R agonism enhances adjustable gastric banding in diet-induced obese rats.

Journal Article (Journal Article)

Bariatric procedures vary in efficacy, but overall are more effective than behavioral and pharmaceutical treatment. Roux-en-Y gastric bypass causes increased secretion of glucagon-like peptide 1 (GLP-1) and reduces body weight (BW) more than adjustable gastric banding (AGB), which does not trigger increased GLP-1 secretion. Since GLP-1-based drugs consistently reduce BW, we hypothesized that GLP-1 receptor (GLP-1R) agonists would augment the effects of AGB. Male Long-Evans rats with diet-induced obesity received AGB implantation or sham surgery. GLP-1R agonism, cannabinoid receptor-1 (CB1-R) antagonism, or vehicle was combined with inflation to evaluate interaction between AGB and pharmacological treatments. GLP1-R agonism reduced BW in both sham and AGB rats (left uninflated) compared with vehicle-treated animals. Subsequent band inflation was ineffective in vehicle-treated rats but enhanced weight loss stimulated by GLP1-R agonism. In contrast, there was no additional BW loss when CB1-R antagonism was given with AGB. We found band inflation to trigger neural activation in areas of the nucleus of the solitary tract known to be targeted by GLP-1R agonism, offering a potential mechanism for the interaction. These data show that GLP-1R agonism, but not CB1-R antagonism, improves weight loss achieved by AGB and suggest an opportunity to optimize bariatric surgery with adjunctive pharmacotherapy.

Full Text

Duke Authors

Cited Authors

  • Habegger, KM; Kirchner, H; Yi, C-X; Heppner, KM; Sweeney, D; Ottaway, N; Holland, J; Amburgy, S; Raver, C; Krishna, R; Müller, TD; Perez-Tilve, D; Pfluger, PT; Obici, S; DiMarchi, RD; D'Alessio, DA; Seeley, RJ; Tschöp, MH

Published Date

  • September 2013

Published In

Volume / Issue

  • 62 / 9

Start / End Page

  • 3261 - 3267

PubMed ID

  • 23775764

Pubmed Central ID

  • PMC3749327

Electronic International Standard Serial Number (EISSN)

  • 1939-327X

Digital Object Identifier (DOI)

  • 10.2337/db13-0117


  • eng

Conference Location

  • United States