The aim was to understand the direct impact of aerobic short-term exercise on lipid metabolism, specifically in regulating the mitochondrial carrier homolog 2 (MTCH2) and how it interferes with lipid metabolism in mesenteric adipose tissue. Swiss mice were divided into three groups: control, sedentary obese, and exercised obese. The obese groups were induced into obesity for fourteen weeks of a high-fat diet, and the trained submitted to seven aerobic exercise sessions. The exercise proved the significant increase of the pPerilipin-1, a hormone-sensitive lipase gene, and modulates lipid metabolism by increasing the expression of and acetyl Co-A carboxylase, perhaps occurring as feedback to regulate lipid metabolism in adipose tissue. In conclusion, we demonstrate, for the first time, how aerobic physical exercise increases transcription in mesenteric adipose tissue. This increase was due to changes in energy demand caused by exercise, confirmed by observing the significant reduction in mesenteric adipose tissue mass in the exercised group. Also, we showed that physical exercise increased the phosphorylative capacity of PLIN1, a protein responsible for the degradation of fatty acids in the lipid droplet, providing acyl and glycerol for cellular metabolism. Although our findings demonstrate evidence of MTCH2 as a protein that regulates lipid homeostasis, scant knowledge exists concerning the signaling of the MTCH2 pathway in regulatingfatty acid metabolism. Therefore, unveiling the means of molecular signaling of MTCH2 demonstrates excellent potential for treating obesity.

中文翻译：

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有氧运动对线粒体载体同源物2的调节及其对肥胖小鼠肠系膜脂肪组织脂质分解代谢和合成代谢活性的影响

目的是了解短期有氧运动对脂质代谢的直接影响，特别是在调节线粒体载体同源物 2 (MTCH2) 方面以及它如何干扰肠系膜脂肪组织中的脂质代谢。瑞士小鼠被分为三组：对照组、久坐肥胖组和运动肥胖组。肥胖组接受十四周的高脂肪饮食，并接受七次有氧运动。该练习证明了激素敏感性脂肪酶基因 pPerilipin-1 的显着增加，并通过增加乙酰辅酶 A 羧化酶的表达来调节脂质代谢，可能作为调节脂肪组织中脂质代谢的反馈而发生。总之，我们首次证明了有氧运动如何增加肠系膜脂肪组织的转录。这种增加是由于运动引起的能量需求的变化，通过观察运动组肠系膜脂肪组织质量的显着减少证实了这一点。此外，我们还发现，体育锻炼增加了 PLIN1 的磷酸化能力，PLIN1 是一种负责脂滴中脂肪酸降解的蛋白质，为细胞代谢提供酰基和甘油。尽管我们的研究结果证明了 MTCH2 作为调节脂质稳态的蛋白质的证据，但关于 MTCH2 通路在调节脂肪酸代谢中的信号传导知之甚少。因此，揭示 MTCH2 的分子信号转导手段展示了治疗肥胖的巨大潜力。