日本大阪都市大学的研究团队发现，线粒体融合蛋白OPA1在下丘脑MC4R神经元中的作用可能有助于解释人类难以抗拒高脂肪食物的原因1。研究表明，缺乏这一蛋白质的小鼠表现出进食增加、体重快速上升的现象，最终导致肥胖1。
研究还揭示了性别在这一过程中的显著影响1。在高脂肪饮食环境下，OPA1在雄性小鼠中的表达增加，但在雌性小鼠中无此变化1。当OPA1蛋白缺乏时，雌性小鼠表现出更明显的肥胖倾向1。此外，抗肥胖药物setmelanotide在对照组及OPA1缺乏的雄性小鼠中能够有效抑制食欲，但在OPA1缺乏的雌性小鼠中的效能明显减弱1。该研究由大阪都市大学人类生活与生态学院教授Shigenobu Matsumura领导，成果已发表在《美国实验生物学学会联合会期刊》2026年第40卷第10期1。
Researchers at Osaka Metropolitan University have identified a mitochondrial protein that could help clarify why humans struggle to avoid high-fat foods.1 The study, led by Professor Shigenobu Matsumura from the university's Faculty of Human Life and Ecology, examined the role of optic atrophy 1 (OPA1) protein in hypothalamic MC4R neurons.1
Mice lacking OPA1 consumed significantly more food and gained weight faster than their healthy counterparts, ultimately developing obesity.1 The research revealed notable sex-based differences in how this protein functions: when exposed to high-fat soybean oil, OPA1 expression increased in male mice but remained unchanged in female mice.1 Female mice deficient in OPA1 showed more pronounced obesity effects compared to males.1 Additionally, the antiobesity drug setmelanotide proved effective in both control and OPA1-deficient male mice, but its appetite-suppressing capacity was significantly diminished in OPA1-deficient female mice.1 The findings were published in The FASEB Journal in 2026, volume 40, issue 10.1
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