大阪都市大学研究团队发现，线粒体融合蛋白OPA1在下丘脑MC4R神经元中可能对食欲控制和防止过度进食起重要作用。[1]由Shigenobu Matsumura教授领导的研究采用基因工程小鼠模型，比较了野生型小鼠与OPA1被特异性移除的小鼠在摄食行为上的差异。[1]实验中，研究人员以豆油作为膳食脂肪来源，观察了小鼠的进食量和体重变化。[1]
研究结果显示，缺乏OPA1的小鼠进食更多、随年龄增长体重增加更快并最终发生肥胖。[1]当在标准饲料和豆油之间自由选择时，OPA1缺乏小鼠消耗更多脂肪并额外增重，这种效应在雌性小鼠中尤其强烈。[1]豆油增加了雄性野生型小鼠的OPA1表达，但在雌性小鼠中未见此增加，提示性别可能影响该蛋白的调节。[1]
在药物测试中，肥胖症治疗药物司美拉诺肽成功降低了对照组及OPA1缺乏雄性小鼠的食欲，但在OPA1缺乏雌性小鼠中抑制食欲的能力明显较弱。[1]这一发现表明OPA1缺乏可能导致某些抗肥胖药物效力降低，尤其是在女性群体中。该研究于2026年8月13日发表在《FASEB期刊》第40卷第10期。[1]
Researchers at Osaka Metropolitan University have identified a mitochondrial protein that appears to play a crucial role in appetite regulation and obesity prevention.[1] The protein, known as optic atrophy 1 (OPA1), is located in hypothalamic MC4R neurons and may hold new insights into why some individuals struggle to control their intake of high-fat foods.[1]
In their study, led by Professor Shigenobu Matsumura, the research team compared mice with normal OPA1 levels to those with the protein selectively removed.[1] Mice lacking OPA1 consumed significantly more food, gained weight faster as they aged, and were more susceptible to obesity.[1] When given a choice between standard feed and soybean oil as a dietary fat source, OPA1-deficient mice consumed more fat and gained additional weight, with this effect being particularly pronounced in female mice.[1] Notably, soybean oil increased OPA1 expression in male wild-type mice but did not produce the same effect in females.[1]
The findings took on additional significance when researchers tested setmelanotide, an obesity medication commonly used to suppress appetite.[1] While the drug successfully reduced food intake in control male mice and OPA1-deficient male mice, it demonstrated markedly reduced appetite-suppressing capability in OPA1-deficient female mice.[1] The research was published in The FASEB Journal on August 13, 2026.[1]