Department of Geriatric Medicine, RWTH Aachen University Hospital, Germany.
Institute for Biomedicine of Aging, Friedrich-Alexander-Universität Erlangen-Nürnberg, Nuremberg, Germany.
Dis Markers. 2019 Jul 1;2019:9140789. doi: 10.1155/2019/9140789. eCollection 2019.
Obesity and inflammation are reportedly associated with the pathogenesis of sarcopenia, which is characterized by age-related loss of skeletal muscle mass. Intramuscular fat deposits have been found to compromise muscle integrity; however, the relevant fat compounds and their roles as mediators of muscular inflammation are not known. The aim of this study was to identify potential correlations between inflammation markers and lipid compounds that accumulate in the quadriceps muscle of previously described Sprague-Dawley (SD) rat model for high-fat diet- (HFD-) induced muscle loss. Six-month-old SD rats were continuously fed a control (CD) or HFD until the age of 21 months. Magnetic resonance imaging (MRI) revealed a significant decline in muscle cross-sectional area in male SD rats as a result of HFD, but not in female rats. Here, we developed a new procedure to quantitatively identify and classify the fatty acid methyl esters (FAMEs) in rats' quadriceps muscles from our former study using gas chromatography-mass spectrometry (GC-MS). Fatty acid analysis revealed accumulation of octadecadienoic (linoleic acid), octadecanoic (stearic acid), and octadecenoic (vaccenic acid) acids exclusively in the quadriceps muscles of male rats. The designated fatty acids were mainly incorporated into triacylglycerols (TAGs) or free fatty acids (FFAs), and their proportions were significantly elevated by consumption of a HFD. Furthermore, the number of resident immune cells and the levels of the chemokines RANTES, MCP-1, and MIP-2 were significantly increased in quadriceps muscle tissue of HFD-fed male, but not female rats. Together, HFD-induced muscle loss in aged male SD rats is associated with greater deposits of long-chain fatty acid esters and increased levels of the inflammatory markers RANTES, MCP-1, and MIP-2 in skeletal muscle tissue. This trend is further reinforced by long-term consumption of a HFD, which may provoke synergistic crosstalk between long-chain fatty acids and inflammatory pathways in sarcopenic muscle.
肥胖和炎症据称与肌肉减少症的发病机制有关，肌肉减少症的特征是与年龄相关的骨骼肌量损失。已经发现肌肉内脂肪沉积会损害肌肉完整性；然而，相关的脂肪化合物及其作为肌肉炎症介质的作用尚不清楚。本研究旨在确定炎症标志物与脂质化合物之间的潜在相关性，这些脂质化合物在先前描述的高脂肪饮食（HFD）诱导的肌肉减少的 Sprague-Dawley（SD）大鼠模型的股四头肌中积累。六个月大的 SD 大鼠连续喂食对照饮食（CD）或 HFD，直至 21 个月大。磁共振成像（MRI）显示 HFD 导致雄性 SD 大鼠的肌肉横截面积显著下降，但雌性大鼠则没有。在这里，我们开发了一种新的程序，使用气相色谱-质谱法（GC-MS）从前一项研究中定量鉴定和分类大鼠股四头肌中的脂肪酸甲酯（FAMEs）。脂肪酸分析显示，十八碳二烯酸（亚油酸）、十八烷酸（硬脂酸）和十八碳烯酸（蓖麻酸）仅在雄性大鼠的股四头肌中积累。指定的脂肪酸主要掺入三酰基甘油（TAGs）或游离脂肪酸（FFAs），并且它们的比例因 HFD 的消耗而显着升高。此外，HFD 喂养的雄性大鼠但不是雌性大鼠的股四头肌组织中常驻免疫细胞的数量和趋化因子 RANTES、MCP-1 和 MIP-2 的水平显着增加。总之，HFD 诱导的老年雄性 SD 大鼠肌肉减少症与骨骼肌组织中长链脂肪酸酯的沉积增加以及炎症标志物 RANTES、MCP-1 和 MIP-2 的水平升高有关。这种趋势因长期摄入 HFD 而进一步增强，这可能会引发肌肉减少症中长链脂肪酸和炎症途径之间的协同串扰。
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