Lipotoxicity plays a key role in the development of both insulin resistance and muscle atrophy in patients with type 2 diabetes
Lipotoxicity plays a key role in the development of both insulin resistance and muscle atrophy in patients with type 2 diabetes
复制标题
脂毒性在2型糖尿病患者胰岛素抵抗和肌肉萎缩的发展中起着关键作用
DOI：
10.1111/obr.12862
复制
发表时间：
2019-09-01
期刊：
影响因子：
8.9
通讯作者：
van Loon, Luc J. C.
中科院分区：
文献类型：
--
作者：
Meex, Ruth C. R.;Blaak, Ellen E.;van Loon, Luc J. C.
在2型糖尿病患者中，胰岛素抵抗和肌肉质量下降通常是同时发生的。大多数2型糖尿病患者超重，肥胖和脂代谢紊乱在这些人的胰岛素抵抗发展中起着重要作用。具体地说，脂肪组织质量增加和功能失调的脂肪组织会导致全身性脂质溢出，并通过改变脂肪因子和细胞因子的分泌而导致轻度炎症。此外，脂肪组织中脂肪酸流量的增加可能有助于增加肝脏和骨骼肌中的脂肪存储，导致肝细胞因子分泌改变，线粒体功能障碍，骨骼肌中胰岛素信号转导受损。最近的研究表明，肥胖和脂肪组织中的脂肪紊乱也会导致肌肉萎缩，这将使胰岛素抵抗和肌肉萎缩成为一枚硬币的两面。不幸的是，脂肪堆积、2型糖尿病和肌肉萎缩之间的确切关系在很大程度上仍未得到探索。本综述的目的是讨论2型糖尿病与肌肉丢失的关系，并讨论器官中脂质积累可能影响外周胰岛素敏感性和肌肉质量的一些关节途径。
Insulin resistance and muscle mass loss often coincide in individuals with type 2 diabetes. Most patients with type 2 diabetes are overweight, and it is well established that obesity and derangements in lipid metabolism play an important role in the development of insulin resistance in these individuals. Specifically, increased adipose tissue mass and dysfunctional adipose tissue lead to systemic lipid overflow and to low-grade inflammation via altered secretion of adipokines and cytokines. Furthermore, an increased flux of fatty acids from the adipose tissue may contribute to increased fat storage in the liver and in skeletal muscle, resulting in an altered secretion of hepatokines, mitochondrial dysfunction, and impaired insulin signalling in skeletal muscle. Recent studies suggest that obesity and lipid derangements in adipose tissue can also lead to the development of muscle atrophy, which would make insulin resistance and muscle atrophy two sides of the same coin. Unfortunately, the exact relationship between lipid accumulation, type 2 diabetes, and muscle atrophy remains largely unexplored. The aim of this review is to discuss the relationship between type 2 diabetes and muscle loss and to discuss some of the joint pathways through which lipid accumulation in organs may affect peripheral insulin sensitivity and muscle mass.