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.