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].