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Habegger, K.M.* ; Kirchner, H.* ; Yi, C.-X. ; Heppner, K.M.* ; Sweeney, D.* ; Ottaway, N.* ; Holland, J.* ; Amburgy, S.* ; Raver, C.* ; Krishna, R.* ; Müller, T.D. ; Perez-Tilve, D.* ; Pfluger, P.T. ; Obici, S.* ; DiMarchi, R.D.* ; D'Alessio, D.A.* ; Seeley, R.J.* ; Tschöp, M.H.

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

Diabetes 62, 3261-3267 (2013)
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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 more than adjustable gastric banding (AGB), which does not trigger increased GLP-1 secretion. Since GLP-1-based drugs consistently reduce body weight, 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 un-inflated) compared to vehicle-treated animals. Subsequent band inflation was ineffective in vehicle-treated rats, but enhanced weight loss stimulated by GLP1-R agonism. In contrast, there were 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 GLP1-R agonism, offering 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.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Glucagon-like Peptide-1 ; Weight-loss ; Food-intake ; Sleeve Gastrectomy ; Brain-stem ; Surgery ; Bypass ; Receptor ; Glucose
Language english
Publication Year 2013
HGF-reported in Year 2013
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Journal Diabetes
Quellenangaben Volume: 62, Issue: 9, Pages: 3261-3267 Article Number: , Supplement: ,
Publisher American Diabetes Association
Publishing Place Alexandria, VA.
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes and Obesity (IDO)
POF-Topic(s) 30201 - Metabolic Health
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502200-001
PubMed ID 23775764
DOI 10.2337/db13-0117
WOS ID WOS:000323421000034
Erfassungsdatum 2013-06-21
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