Duran Miguel, Willis Jennifer R, Dalvi Nilay, Fokakis Zoe, Virkus Sonja A, Hardaway J Andrew
Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Endocrinology. 2025 Feb 5;166(3). doi: 10.1210/endocr/bqaf019.
Understanding the detailed mechanism of action of glucagon-like peptide 1 receptor (GLP-1R) agonists on distinct topographic and genetically defined brain circuits is critical for improving the efficacy and mitigating adverse side effects of these compounds. In this mini-review, we propose that the central nucleus of the amygdala (CeA) is a critical mediator of GLP-1R agonist-driven hypophagia. Here, we review the extant literature demonstrating CeA activation via GLP-1R agonists across multiple species and through multiple routes of administration. The precise role of GLP-1Rs within the CeA is unclear but the site-specific GLP-1Rs may mediate distinct behavioral and physiological hallmarks of GLP-1R agonists on food intake. Thus, we propose important novel directions and methods to test the role of the CeA in mediating GLP-1R actions.
了解胰高血糖素样肽1受体（GLP-1R）激动剂对不同地形和基因定义的脑回路的详细作用机制，对于提高这些化合物的疗效和减轻副作用至关重要。在这篇小型综述中，我们提出杏仁核中央核（CeA）是GLP-1R激动剂驱动的食欲减退的关键介质。在此，我们回顾了现有文献，这些文献表明通过多种给药途径，GLP-1R激动剂可激活多个物种的CeA。CeA内GLP-1R的确切作用尚不清楚，但位点特异性GLP-1R可能介导GLP-1R激动剂对食物摄入的不同行为和生理特征。因此，我们提出了重要的新方向和方法来测试CeA在介导GLP-1R作用中的作用。
