Ruan Jinxue, Zhang Yuanyuan, Yuan Jing, Xin Leilei, Xia Jihan, Liu Nan, Mu Yulian, Chen Yaoxing, Yang Shulin, Li Kui
State Key Laboratory of Animal Nutrition, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, No. 2 Yuanmingyuan West Road, Beijing, 100193, PR China; Jilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Science, Jilin University, Changchun, 130012, PR China.
College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing, 100193, PR China.
Mol Cell Endocrinol. 2016 Apr 15;425:123-32. doi: 10.1016/j.mce.2016.02.001. Epub 2016 Feb 2.
Skeletal muscle is as an important regulator of blood glucose and glycolipid metabolism and is closely related to motor ability. The underlying mechanisms by which dietary ectopic lipids in skeletal muscle prevents muscle growth remain elusive. We utilized miniature Bama swine as a model to mimic human obesity using prolonged dietary induction. After 23 months on a high-fat, high-sucrose diet, metabolic disorders were induced in the animals, which exhibited increased body weight, extensive lipid deposition in the skeletal muscle and amyotrophy. Microarray profiles demonstrated the up-regulation of genes related to fat deposition and muscle growth inhibition. We outline a clear potential pathway that in combination with increased 11β-hydroxysteroid dehydrogenase type 1, promotes expression of a major inhibitor, myostatin, by converting corticosterone to cortisol, which leads to the growth inhibition of skeletal muscle. This research provides new insights into the treatment of muscle diseases induced by obesity.
骨骼肌是血糖和糖脂代谢的重要调节因子，与运动能力密切相关。骨骼肌中饮食异位脂质阻止肌肉生长的潜在机制仍不清楚。我们利用小型巴马猪作为模型，通过长期饮食诱导来模拟人类肥胖。在高脂、高蔗糖饮食23个月后，诱导动物出现代谢紊乱，表现为体重增加、骨骼肌广泛脂质沉积和肌萎缩。基因芯片分析表明与脂肪沉积和肌肉生长抑制相关的基因上调。我们勾勒出一条明确的潜在途径，即与11β-羟基类固醇脱氢酶1型增加相结合，通过将皮质酮转化为皮质醇来促进主要抑制剂肌肉生长抑制素的表达，从而导致骨骼肌生长抑制。这项研究为肥胖引起的肌肉疾病的治疗提供了新的见解。
