剑桥大学研究团队发现了一个看似矛盾的生物学现象：激活和阻断同一种受体——GIP受体——都能达到减肥效果，但作用原理截然不同 1。研究表明，在脑干中激活GIP受体可以降低食欲从而导致体重下降，而在下丘脑中阻断GIP受体则通过释放控制饱腹感的"制动器"来促进减肥 1。
这一发现已发表在《自然·代谢》期刊上 1，为现有多种肥胖药物的相似疗效提供了生物学解释。目前市面上的部分药物（包括Mounjaro和Zepbound）通过激活GIPR发挥作用，而正处于第3阶段临床试验的MariTide等药物则通过阻断GIPR并同时激活GLP-1受体来实现减肥效果 1。剑桥大学的Dr. Jo Lewis指出："了解哪些脑回路对这些药物有反应以及它们如何反应，可以帮助我们设计更好的药物，以更少的副作用产生更多的减肥效果" 1。这项研究表明，GIP靶向治疗与GLP-1药物的联合使用可能会产生更强的疗效 1。
Researchers at Cambridge University have discovered that activating and blocking the same brain receptor can both lead to weight loss, but through fundamentally different biological pathways.1 Specifically, activating GIP receptors in the brainstem reduces appetite and promotes weight loss, while blocking GIP receptors in the hypothalamus triggers weight reduction by releasing the "brake" on satiety signals.1
The findings, published in Nature Metabolism, help explain why different obesity medications achieve similar weight loss outcomes despite operating through opposite mechanisms.1 The research suggests that certain drugs like Mounjaro and Zepbound activate GIPR, whereas medications such as MariTide—currently in phase 3 clinical trials—block it while also activating GLP-1 receptors.1 According to Dr. Jo Lewis, "Understanding which brain circuits respond to these drugs and how they respond can help us design better medicines that produce greater weight loss effects with fewer side effects."1 This dual-pathway understanding opens the possibility of combining GIP-targeted therapies with existing GLP-1 drugs to achieve more potent results.1
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