Coles C A
Murdoch Children's Research Institute, Royal Children's Hospital, Flemington Rd, Parkville, Melbourne, VIC, 3052, Australia.
Adv Exp Med Biol. 2016;900:133-60. doi: 10.1007/978-3-319-27511-6_6.
Adipose tissue not only functions as a reserve to store energy but has become of major interest as an endocrine organ, releasing signalling molecules termed adipokines which impact on other tissues, such as skeletal muscle. Adipocytes, within skeletal muscle and adipose tissue, secrete adipokines to finely maintain the balance between feed intake and energy expenditure. This book chapter focuses on the three adipokines, adiponectin, leptin and IL-6, which have potent effects on skeletal muscle during rest and exercise. Similarly, adiponectin, leptin and IL-6 enhance glucose uptake and increase fatty acid oxidation in skeletal muscle. Fatty acid oxidation is increased through activation of AMPK (adenosine monophosphate-activated protein kinase signalling) causing phosphorylation and inhibition of ACC (acetyl-coenzyme A carboxylase), decreasing availability of malonyl CoA. Leptin and adiponectin also control feed intake via AMPK signalling in the hypothalamus. Adipokines function to maintain energy homeostasis, however, when feed intake exceeds energy expenditure adipokines can become dysregulated causing lipotoxicity in skeletal muscle and metabolic disease can prevail. Cross-talk between adipocytes and skeletal muscle via correct control by adipokines is important in controlling energy homeostasis during rest and exercise and can help prevent metabolic disease.
脂肪组织不仅作为储存能量的储备器官发挥作用,而且作为一个内分泌器官已引起了人们的极大兴趣,它能释放被称为脂肪因子的信号分子,这些分子会影响其他组织,如骨骼肌。骨骼肌和脂肪组织内的脂肪细胞分泌脂肪因子,以精确维持食物摄入与能量消耗之间的平衡。本章重点介绍三种脂肪因子,脂联素、瘦素和白细胞介素-6,它们在休息和运动期间对骨骼肌有显著影响。同样,脂联素、瘦素和白细胞介素-6可增强骨骼肌对葡萄糖的摄取并增加脂肪酸氧化。通过激活AMPK(单磷酸腺苷激活的蛋白激酶信号通路)导致乙酰辅酶A羧化酶(ACC)磷酸化并受到抑制,减少丙二酰辅酶A的可用性,从而增加脂肪酸氧化。瘦素和脂联素还通过下丘脑的AMPK信号通路控制食物摄入。脂肪因子的功能是维持能量稳态,然而,当食物摄入量超过能量消耗时,脂肪因子可能会失调,导致骨骼肌出现脂毒性,代谢疾病可能会盛行。脂肪细胞与骨骼肌之间通过脂肪因子的正确调控进行相互作用,对于在休息和运动期间控制能量稳态很重要,并且有助于预防代谢疾病。