| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3001520 | Molecular Metabolism | 2015 | 6 Pages |
•GLP-1 levels associate with food cue-induced brain activity in the orbitofrontal cortex, a major reward area.•While obese persons are brain insulin-resistant in the orbitofrontal cortex, they still respond to GLP-1.•Postprandial GLP-1 release may alter reward processes in the orbitofrontal cortex to support the termination of food intake.
ObjectiveGlucagon-like peptide-1 (GLP-1) is released into the bloodstream after food intake. In addition to stimulating insulin release, it causes satiety and contributes to the termination of food intake. In this study, we investigated whether endogenous GLP-1 affects food-related brain activity and hunger.MethodsTwenty-four volunteers (12 lean; 12 obese) underwent a 75 g oral glucose tolerance test that promotes GLP-1 secretion. Food cue-induced brain activity was assessed by functional magnetic resonance imaging and GLP-1 concentrations were measured before, 30, and 120 min after glucose intake.ResultsThe significant increase in GLP-1 levels negatively correlated with a change in the food cue-induced brain activity in the orbitofrontal cortex, a major reward area. This association was independent of simultaneous alterations in insulin and glucose concentrations. The association was present in lean and overweight participants. By contrast, postprandial insulin changes were associated with orbitofrontal activations in lean individuals only.ConclusionsThe postprandial release of GLP-1 might alter reward processes in the orbitofrontal cortex and might thereby support the termination of food intake and reduce hunger. While obese persons showed brain insulin resistance, no GLP-1 resistance was observed. Our study provides novel insight into the central regulation of food intake by the incretin hormone GLP-1.
