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《Science》揭新发现:神秘信号通路居然与肥胖高度相关
GLP1减重宝典· 2026-01-01 08:32
以下文章来源于肥胖世界ObesityWorld ,作者欢迎订阅 肥胖世界ObesityWorld . 《肥胖世界》Obesity World - 同步传真肥胖及代谢国际新学术进展,为医学减重临床、教研人员搭建一座与国际接轨的桥梁,「每医健」旗下内容平台。 近年来,减肥药物的快速发展正深刻改变医疗行业,不仅实现了持久的体重控制,还在心血管健康、血糖平衡以及血压和胆固醇管理方面展现 出显著益处。此次新研究为开发新靶点药物打开了大门,这些靶点未来既可单独应用,也能与现有减重药物联用,从而更有效地控制食欲。 体重受遗传和环境因素双重影响。Zhang博士指出,由于饮食和生活方式差异巨大,直接在人类中寻找导致肥胖的基因变异极具挑战。因此, 研究团队采用了AMM(自动减数分裂定位)增强的遗传学方法,以更好地解析肥胖的遗传基础。 AMM(Automated Meiotic Mapping)是一项结合遗传学与机器学习的新技术,能够高效定位导致特定表型的基因突变。该技术由UTSW团队 与诺贝尔奖获得者Bruce Beutler博士共同开发,通过分析基因型与表型数据,利用统计和人工智能手段,快速筛查出与性状相关的遗传变异。 为进一 ...
《Science》最新揭示:这个神秘信号通路,竟与肥胖关系密切
GLP1减重宝典· 2025-10-13 13:09
Core Insights - The article discusses a groundbreaking research published in "Science" that reveals a new signaling pathway in the brain's neurons, which plays a crucial role in appetite regulation and could lead to new anti-obesity strategies. Currently, obesity affects approximately 40% of adults in the U.S. and over 1 billion people globally [6][7]. Group 1: Research Findings - The research team, led by Dr. Zhao Zhang, discovered a previously unknown signaling pathway in the cilia of brain neurons that regulates appetite, presenting a new breakthrough for weight loss treatments [7]. - The rapid development of weight loss medications is transforming the healthcare industry, achieving lasting weight control and showing significant benefits in cardiovascular health, blood sugar balance, and management of blood pressure and cholesterol [7]. - The study utilized Automated Meiotic Mapping (AMM), a combination of genetics and machine learning, to efficiently locate gene mutations associated with obesity [8]. Group 2: Genetic Insights - The research identified the Gpr45 gene as central to weight regulation, with mutations leading to obesity in mice due to increased food intake [8]. - GPR45 protein is highly expressed in hypothalamic neurons and is involved in transporting Gαs protein to primary cilia, activating the MC4R signaling pathway to regulate appetite [9]. - Current medications targeting MC4R are limited to specific genetic mutations and do not apply to the broader obesity population, highlighting the potential for developing drugs that enhance GPR45 activity for wider treatment options [9].