美国国立卫生研究院资助的一项研究发现，新型口服GLP-1药物通过作用于大脑奖赏系统来减少进食欲望1。弗吉尼亚大学研究团队在小鼠实验中发现，包括已获美国食品药品监督管理局批准的orforglipron和实验性药物danuglipron在内的口服GLP-1类药物，能够激活中央杏仁核并降低进食时的多巴胺释放1。这些发现已发表在《自然》杂志2026年第654卷第8120期上1。
研究人员Ali Guler博士表示："我们已知GLP-1药物可以抑制由能量需求驱动的进食行为。现在似乎口服小分子GLP-1类药物也通过激活大脑奖赏回路来减少享乐性进食"1。这一发现揭示了这类药物影响大脑奖赏回路的新机制，可能为理解食物渴望和治疗物质成瘾提供新思路1。
Researchers funded by the National Institutes of Health have identified a new mechanism by which oral GLP-1 medications reduce food cravings in the brain 1. A team from the University of Virginia discovered that drugs in this class, including the FDA-approved orforglipron and the experimental danuglipron, activate the central amygdala while simultaneously lowering dopamine release during eating 1. This finding suggests that oral GLP-1 drugs work not only to suppress hunger driven by energy needs, but also to diminish pleasure-based eating by modulating the brain's reward circuitry 1.
According to Dr. Ali Guler of the research team, "We already knew that GLP-1 drugs can suppress eating behavior driven by energy demands. Now it appears that oral small-molecule GLP-1 drugs also reduce hedonic eating by activating the brain's reward circuit" 1. The study was conducted on mice and reveals a previously unknown pathway through which these medications influence appetite control 1. The research was published in Nature in July 2026, volume 654, issue 8120 1. These findings may offer new insights into understanding food cravings and potentially inform approaches to treating substance addiction 1.
评论
还没有评论，欢迎留下第一条。