肌动蛋白
FNDC5
内科学
内分泌学
脂肪因子
FGF21型
肌生成抑制素
脂肪组织
骨骼肌
旁分泌信号
白色脂肪组织
医学
卵泡抑素
肥胖
生物
瘦素
脂联素
胰岛素抵抗
细胞生物学
胰岛素
成纤维细胞生长因子
受体
细胞外基质
纤维连接蛋白
作者
Amaia Rodríguez,Sara Becerril,Silvia Ezquerro,Leire Méndez‐Giménez,Gema Frühbeck
摘要
Abstract Skeletal muscle is the largest organ determining whole‐body insulin sensitivity and metabolic homoeostasis. Adaptive changes of skeletal muscle in response to physical activity include adjustments in the production and secretion of muscle‐derived bioactive factors, known as myokines, such as myostatin, IL ‐4, IL ‐6, IL ‐7 and IL ‐15, myonectin, follistatin‐like 1 or leukaemia inhibitory factor. These myokines not only act locally in the muscle in an autocrine/paracrine manner, but also are released to the bloodstream as endocrine factors to regulate physiological processes in other tissues. Irisin, derived from the cleavage of FNDC 5 protein, constitutes a myokine that induces myogenesis and fat browning (switch of white adipocytes to brown fat‐like cells) together with a concomitant increase in energy expenditure. Besides being a target for irisin actions, the adipose tissue also constitutes a production site of FNDC 5. Interestingly, irisin secretion from subcutaneous and visceral fat depots is decreased by long‐term exercise training and fasting, suggesting a discordant regulation of FNDC 5/irisin in skeletal muscle and adipose tissue. Accordingly, our group has recently reported that the adipokine leptin differentially regulates FNDC 5/irisin expression in skeletal muscle and fat, confirming the crosstalk between both tissues. Moreover, irisin secretion and function are regulated by other myokines, such as follistatin or myostatin, as well as by other adipokines, including fibroblast growth factor 21 and leptin. Taken together, myokines have emerged as novel molecular mediators of fat browning and their activity can be modulated by adipokines, confirming the crosstalk between skeletal muscle and adipose tissue to regulate thermogenesis and energy expenditure.
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