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register hereMales are at higher risk for developing metabolic dysfunction-associated steatohepatitis (MASH) than females; however, mechanisms mediating sexual dimorphism in MASH development are not completely understood. Nutrition-based mouse models suggest that dysregulated fatty acid biosynthesis promotes MASH.

在此登记男性患代谢功能障碍相关脂肪性肝炎（MASH）的风险高于女性；然而，在MASH发育中介导性二态性的机制尚不完全清楚。基于营养的小鼠模型表明，脂肪酸生物合成失调会促进MASH。

Drugs recapitulate MASH without diet variabilities. This brief report investigates associations of sexual dimorphism with male susceptibility to MASH utilizing a drug-induced MASH model and focuses on very long chain fatty acid biosynthesis pathways. We assessed male and female mouse livers 5-and 15-weeks following MASH induction by immunizations and age-matched un-immunized controls utilizing western blot.

。本简要报告利用药物诱导的MASH模型研究了性别二态性与男性对MASH易感性的关系，并重点研究了超长链脂肪酸的生物合成途径。我们通过免疫接种和使用蛋白质印迹的年龄匹配的未免疫对照评估了MASH诱导后5周和15周的雄性和雌性小鼠肝脏。

Our results suggest that PPAR alpha and CYP4a12a protect females while CYP4v2 does not protect males from MASH development. Our results have important implications for understanding sexual dimorphism in the pathogenesis of MASH..

我们的研究结果表明，PPARα和CYP4a12a可以保护雌性，而CYP4v2不能保护雄性免受MASH发育的影响。我们的结果对于理解MASH发病机理中的性别二态性具有重要意义。。