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游泳通过激活骨骼肌 PPARα 预防去卵巢诱导的肥胖。

Swimming's prevention of ovariectomy-induced obesity through activation of skeletal-muscle PPARα.

机构信息

Department of Life Science, Mokwon University, Daejeon, Korea.

出版信息

Int J Sport Nutr Exerc Metab. 2012 Feb;22(1):1-10. doi: 10.1123/ijsnem.22.1.1.

DOI:10.1123/ijsnem.22.1.1
PMID:22248494
Abstract

Ovariectomy leads to weight gain primarily in the form of adipose tissue in rodents. The authors investigated whether swimming improves ovariectomy-induced obesity through activation of peroxisome proliferator-activated receptor α (PPARα) in the skeletal muscle of female ovariectomized (OVX) mice, an animal model of postmenopausal women. Female mice were randomly divided into 3 groups (n=8/group): a sedentary sham-operated group, a sedentary OVX group, and a swim-trained OVX group. After mice were subjected to swim training or kept sedentary for 6 wk, the authors studied the effects of swimming on not only bodyweight gain, white adipose tissue (WAT) mass, adipocyte size, and skeletal-muscle lipid accumulation but also the expression of skeletal-muscle PPARα target genes. Sedentary OVX mice had significantly higher body weight and WAT than sedentary sham mice. However, swim training reduced body-weight gain, WAT mass, and adipocyte size of OVX mice. Swim-trained OVX mice had significantly lower levels of serum triglycerides and total cholesterol than sedentary OVX mice. Lipid accumulation in skeletal muscle was also markedly decreased by swimming. Concomitantly, swim training significantly increased mRNA levels of skeletal-muscle PPARα and its target enzymes, as well as uncoupling protein 3 (UCP3) responsible for fatty-acid oxidation. These results suggest that swimming can effectively prevent weight gain, adiposity, adipocyte hypertrophy, and lipid disorders caused by ovariectomy, in part through the activation of PPARα and UCP3, in the skeletal muscle of female mice and may contribute to the alleviation of metabolic syndrome, including obesity, hyperlipidemia, and Type 2 diabetes in postmenopausal women.

摘要

卵巢切除术导致啮齿动物主要以脂肪组织的形式增加体重。作者研究了游泳是否通过激活去卵巢雌性小鼠(绝经后女性的动物模型)骨骼肌中的过氧化物酶体增殖物激活受体α (PPARα) 来改善卵巢切除术引起的肥胖。将雌性小鼠随机分为 3 组(每组 8 只):久坐假手术组、久坐去卵巢组和游泳训练去卵巢组。在小鼠进行游泳训练或保持久坐 6 周后,作者研究了游泳对体重增加、白色脂肪组织 (WAT) 质量、脂肪细胞大小和骨骼肌脂质积累的影响,以及骨骼肌 PPARα 靶基因的表达。久坐去卵巢小鼠的体重和 WAT 明显高于久坐假手术小鼠。然而,游泳训练减少了去卵巢小鼠的体重增加、WAT 质量和脂肪细胞大小。游泳训练的去卵巢小鼠的血清甘油三酯和总胆固醇水平明显低于久坐去卵巢小鼠。游泳也明显减少了骨骼肌中的脂质积累。同时,游泳训练显著增加了骨骼肌中 PPARα 及其靶酶的 mRNA 水平,以及负责脂肪酸氧化的解偶联蛋白 3 (UCP3)。这些结果表明,游泳可以通过激活 PPARα 和 UCP3 有效预防去卵巢引起的体重增加、肥胖、脂肪细胞肥大和脂质紊乱,这可能有助于缓解代谢综合征,包括绝经后女性的肥胖、高血脂和 2 型糖尿病。

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