2023年2月17日,《细胞研究》杂志在线发表了清华大学王一国等研究人员的合作成果。该研究发现,famsin是一种新的肠道分泌激素,通过与其受体OLFR796结合,有助于代谢适应禁食。
研究人员发现了一种新的激素famsin,它由肠道分泌,促进代谢适应禁食。在机制上,famsin在禁食期间从单通道跨膜蛋白Gm11437脱落,然后结合OLFR796,这是一种嗅觉受体,进而激活细胞内钙动员。这一famin-OLFR796信号轴促进糖异生和生酮作用的能量动员,以及在禁食期间的能量保存。此外,通过抗体中和famsin改善糖尿病模型的血糖谱,这确定了famsin作为治疗糖尿病的潜在治疗靶点。因此,这些研究结果表明,肠和其他器官之间通过famin-OLFR796信号轴的通信对于禁食的代谢适应至关重要。
据了解,肠道负责营养吸收,并在进食过程中协调不同器官的代谢,这一过程部分由肠道源性激素控制。然而,目前尚不清楚肠道是否在禁食期间的代谢中发挥重要作用。
附:英文原文
Title: Famsin, a novel gut-secreted hormone, contributes to metabolic adaptations to fasting via binding to its receptor OLFR796
Author: Long, Aijun, Liu, Yang, Fang, Xinlei, Jia, Liangjie, Li, Zhiyuan, Hu, Jiang, Wu, Shuang, Chen, Chao, Huang, Ping, Wang, Yiguo
Issue&Volume: 2023-02-17
Abstract: The intestine is responsible for nutrient absorption and orchestrates metabolism in different organs during feeding, a process which is partly controlled by intestine-derived hormones. However, it is unclear whether the intestine plays an important role in metabolism during fasting. Here we have identified a novel hormone, famsin, which is secreted from the intestine and promotes metabolic adaptations to fasting. Mechanistically, famsin is shed from a single-pass transmembrane protein, Gm11437, during fasting and then binds OLFR796, an olfactory receptor, to activate intracellular calcium mobilization. This famsin-OLFR796 signaling axis promotes gluconeogenesis and ketogenesis for energy mobilization, and torpor for energy conservation during fasting. In addition, neutralization of famsin by an antibody improves blood glucose profiles in diabetic models, which identifies famsin as a potential therapeutic target for treating diabetes. Therefore, our results demonstrate that communication between the intestine and other organs by a famsin-OLFR796 signaling axis is critical for metabolic adaptations to fasting.
DOI: 10.1038/s41422-023-00782-7
Source: https://www.nature.com/articles/s41422-023-00782-7
Cell Research:《细胞研究》,创刊于1990年。隶属于施普林格·自然出版集团,最新IF:20.057
官方网址:https://www.nature.com/cr/
投稿链接:https://mts-cr.nature.com/cgi-bin/main.plex