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高脂血症小鼠肌肉力量增强及其与脂肪酸氧化能力增加的关系。

Enhanced Muscle Strength in Dyslipidemic Mice and Its Relation to Increased Capacity for Fatty Acid Oxidation.

机构信息

Department of Biochemistry, Medical University of Gdansk, 80-211 Gdansk, Poland.

Department of Pharmaceutical Biochemistry, Medical University of Gdansk, 80-211 Gdansk, Poland.

出版信息

Int J Mol Sci. 2021 Nov 12;22(22):12251. doi: 10.3390/ijms222212251.

DOI:10.3390/ijms222212251
PMID:34830135
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8620496/
Abstract

Dyslipidemia is commonly linked to skeletal muscle dysfunction, accumulation of intramyocellular lipids, and insulin resistance. However, our previous research indicated that dyslipidemia in apolipoprotein E and low-density lipoprotein receptor double knock-out mice (ApoE/LDLR -/-) leads to improvement of exercise capacity. This study aimed to investigate in detail skeletal muscle function and metabolism in these dyslipidemic mice. We found that ApoE/LDLR -/- mice showed an increased grip strength as well as increased troponins, and Mhc2 levels in skeletal muscle. It was accompanied by the increased skeletal muscle mitochondria numbers (judged by increased citrate synthase activity) and elevated total adenine nucleotides pool. We noted increased triglycerides contents in skeletal muscles and increased serum free fatty acids (FFA) levels in ApoE/LDLR -/- mice. Importantly, Ranolazine mediated inhibition of FFA oxidation in ApoE/LDLR -/- mice led to the reduction of exercise capacity and total adenine nucleotides pool. Thus, this study demonstrated that increased capacity for fatty acid oxidation, an adaptive response to dyslipidemia leads to improved cellular energetics that translates to increased skeletal muscle strength and contributes to increased exercise capacity in ApoE/LDLR -/- mice.

摘要

血脂异常通常与骨骼肌功能障碍、细胞内脂质堆积和胰岛素抵抗有关。然而，我们之前的研究表明，载脂蛋白 E 和低密度脂蛋白受体双敲除小鼠（ApoE/LDLR -/-）的血脂异常导致运动能力的提高。本研究旨在详细研究这些血脂异常小鼠的骨骼肌功能和代谢。我们发现 ApoE/LDLR -/- 小鼠的握力增强，骨骼肌中的肌钙蛋白和 MHC2 水平升高。同时，骨骼肌中线粒体数量增加（通过柠檬酸合酶活性判断），总腺嘌呤核苷酸池升高。我们注意到 ApoE/LDLR -/- 小鼠的骨骼肌中甘油三酯含量增加，血清游离脂肪酸（FFA）水平升高。重要的是，雷诺嗪抑制 ApoE/LDLR -/- 小鼠的游离脂肪酸氧化，导致运动能力和总腺嘌呤核苷酸池减少。因此，本研究表明，脂肪酸氧化能力的增加是对血脂异常的适应性反应，导致细胞能量代谢的改善，从而增强骨骼肌力量，并有助于 ApoE/LDLR -/- 小鼠运动能力的提高。

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