Research Center for Physical Fitness, Sports and Health, Toyohashi University of Technology, 1-1 Hibarigaoka, Tenpaku-cho, Toyohashi 441-8580, Japan.
Int J Endocrinol. 2013;2013:204164. doi: 10.1155/2013/204164. Epub 2013 Apr 11.
In normal aging, changes in the body composition occur that result in a shift toward decreased muscle mass and increased fat mass. The loss of muscle mass that occurs with aging is termed sarcopenia and is an important cause of frailty, disability, and loss of independence in older adults. Age-related changes in the body composition as well as the increased prevalence of obesity determine a combination of excess weight and reduced muscle mass or strength, recently defined as sarcopenic obesity. Weight gain increases total/abdominal fat, which, in turn, elicits inflammation and fatty infiltration in muscle. Sarcopenic obesity appears to be linked with the upregulation of TNF-α, interleukin (IL)-6, leptin, and myostatin and the downregulation of adiponectin and IL-15. Multiple combined exercise and mild caloric restriction markedly attenuate the symptoms of sarcopenic obesity. Intriguingly, the inhibition of myostatin induced by gene manipulation or neutralizing antibody ameliorates sarcopenic obesity via increased skeletal muscle mass and improved glucose homeostasis. In this review, we describe the possible influence of endocrinal changes with age on sarcopenic obesity.
在正常衰老过程中，身体成分会发生变化，导致肌肉量减少和脂肪量增加。随着年龄的增长而发生的肌肉量减少称为肌肉减少症，是老年人虚弱、残疾和丧失独立性的重要原因。身体成分的年龄相关性变化以及肥胖的普遍增加决定了超重和肌肉量或力量减少的结合，最近被定义为肌少症性肥胖。体重增加会增加总/腹部脂肪，这反过来又会引发肌肉炎症和脂肪浸润。肌少症性肥胖似乎与 TNF-α、白细胞介素 (IL)-6、瘦素和肌肉生长抑制素的上调以及脂联素和 IL-15 的下调有关。多种联合运动和轻度热量限制可显著减轻肌少症性肥胖的症状。有趣的是，通过基因操作或中和抗体抑制肌肉生长抑制素可通过增加骨骼肌质量和改善葡萄糖稳态来改善肌少症性肥胖。在这篇综述中，我们描述了年龄相关的内分泌变化对肌少症性肥胖的可能影响。
