Heni Martin, Kullmann Stephanie, Gallwitz Baptist, Häring Hans-Ulrich, Preissl Hubert, Fritsche Andreas
Department of Internal Medicine, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, Eberhard Karls University Tübingen, Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany; German Center for Diabetes Research (DZD e.V.), Tübingen, Germany.
Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany; German Center for Diabetes Research (DZD e.V.), Tübingen, Germany.
Mol Metab. 2015 Sep 30;4(12):971-6. doi: 10.1016/j.molmet.2015.09.007. eCollection 2015 Dec.
Glucagon-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.
Twenty-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.
The 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.
The 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.
胰高血糖素样肽-1（GLP-1）在进食后释放到血液中。除了刺激胰岛素释放外，它还会引起饱腹感并有助于终止进食。在本研究中，我们调查了内源性GLP-1是否会影响与食物相关的大脑活动和饥饿感。
24名志愿者（12名瘦者；12名肥胖者）接受了促进GLP-1分泌的75g口服葡萄糖耐量试验。通过功能磁共振成像评估食物线索诱导的大脑活动，并在葡萄糖摄入前、30分钟和120分钟后测量GLP-1浓度。
GLP-1水平的显著升高与主要奖赏区域眶额皮质中食物线索诱导的大脑活动变化呈负相关。这种关联独立于胰岛素和葡萄糖浓度的同时变化。这种关联在瘦者和超重参与者中均存在。相比之下，餐后胰岛素变化仅与瘦者的眶额皮质激活有关。
餐后GLP-1的释放可能会改变眶额皮质中的奖赏过程，从而可能有助于终止进食并减少饥饿感。虽然肥胖者表现出脑胰岛素抵抗，但未观察到GLP-1抵抗。我们的研究为肠促胰岛素激素GLP-1对食物摄入的中枢调节提供了新的见解。
