Sarcopenic obesity or obese sarcopenia: A cross talk between age-associated adipose tissue and skeletal muscle inflammation as a main mechanism of the pathogenesis

被引:481
|
作者
Kalinkovich, Alexander [1 ]
Livshits, Gregory [1 ]
机构
[1] Tel Aviv Univ, Sackler Fac Med, Dept Anat & Anthropol, Human Populat Biol Res Unit, Tel Aviv, Israel
基金
以色列科学基金会;
关键词
Age; Obesity; Sarcopenia; Sarcopenic obesity; Inflammation; Adipose tissue; Skeletal muscle; EPITHELIUM-DERIVED FACTOR; GROWTH-FACTOR; 21; METABOLICALLY HEALTHY OBESITY; LOW-GRADE INFLAMMATION; DIET-INDUCED OBESITY; BONE MORPHOGENETIC PROTEIN-7; CELLS PROMOTE INFLAMMATION; INDUCED INSULIN-RESISTANCE; OXIDATIVE GENE-EXPRESSION; FATTY-ACID OXIDATION;
D O I
10.1016/j.arr.2016.09.008
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Sarcopenia, an age-associated decline in skeletal muscle mass coupled with functional deterioration, may be exacerbated by obesity leading to higher disability, frailty, morbidity and mortality rates. In the combination of sarcopenia and obesity, the state called sarcopenic obesity (SOB), some key age and obesity-mediated factors and pathways may aggravate sarcopenia. This review will analyze the mechanisms underlying the pathogenesis of SOB. In obese adipose tissue (AT), adipocytes undergo hypertrophy, hyperplasia and activation resulted in accumulation of pro-inflammatory macrophages and other immune cells as well as dysregulated production of various adipokines that together with senescent cells and the immune cell-released cytokines and chemokines create a local pro-inflammatory status. In addition, obese AT is characterized by excessive production and disturbed capacity to store lipids, which accumulate ectopically in skeletal muscle. These intramuscular lipids and their derivatives induce mitochondria( dysfunction characterized by impaired beta-oxidation capacity and increased reactive oxygen species formation providing lipotoxic environment and insulin resistance as well as enhanced secretion of some pro-inflammatory myokines capable of inducing muscle dysfunction by auto/paracrine manner. In turn, by endocrine manner, these myokines may exacerbate AT inflammation and also support chronic low grade systemic inflammation (inflammaging), overall establishing a detrimental vicious circle maintaining AT and skeletal muscle inflammation, thus triggering and supporting SOB development. Under these circumstances, we believe that AT inflammation dominates over skeletal muscle inflammation. Thus, in essence, it redirects the vector of processes from "sarcopenia -> obesity" to "obesity -> sarcopenia". We therefore propose that this condition be defined as "obese sarcopenia", to reflect the direction of the pathological pathway. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:200 / 221
页数:22
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