Mechanism of increased risk of insulin resistance in aging skeletal muscle

Abstract As age increases, the risk of developing type 2 diabetes increases, which is associated with senile skeletal muscle dysfunction. During skeletal muscle aging, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, modified activity of insul...

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Main Authors: Jian Shou, Pei-Jie Chen, Wei-Hua Xiao
Format: Article
Language:English
Published: BMC 2020-02-01
Series:Diabetology & Metabolic Syndrome
Subjects:
Online Access:https://doi.org/10.1186/s13098-020-0523-x
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spelling doaj-916f28731a1244dcabb0f48329e1d7152021-02-14T12:06:43ZengBMCDiabetology & Metabolic Syndrome1758-59962020-02-0112111010.1186/s13098-020-0523-xMechanism of increased risk of insulin resistance in aging skeletal muscleJian Shou0Pei-Jie Chen1Wei-Hua Xiao2School of Kinesiology, Shanghai University of SportSchool of Kinesiology, Shanghai University of SportSchool of Kinesiology, Shanghai University of SportAbstract As age increases, the risk of developing type 2 diabetes increases, which is associated with senile skeletal muscle dysfunction. During skeletal muscle aging, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, modified activity of insulin sensitivity regulatory enzymes, endoplasmic reticulum stress, decreased autophagy, sarcopenia and over-activated renin-angiotensin system may occur. These changes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during skeletal muscle aging. This review of the mechanism of the increased risk of insulin resistance during skeletal muscle aging will provide a more comprehensive explanation for the increased incidence of type 2 diabetes in elderly individuals, and will also provide a more comprehensive perspective for the prevention and treatment of type 2 diabetes in elderly populations.https://doi.org/10.1186/s13098-020-0523-xSkeletal muscle agingInsulin resistanceMechanism
collection DOAJ
language English
format Article
sources DOAJ
author Jian Shou
Pei-Jie Chen
Wei-Hua Xiao
spellingShingle Jian Shou
Pei-Jie Chen
Wei-Hua Xiao
Mechanism of increased risk of insulin resistance in aging skeletal muscle
Diabetology & Metabolic Syndrome
Skeletal muscle aging
Insulin resistance
Mechanism
author_facet Jian Shou
Pei-Jie Chen
Wei-Hua Xiao
author_sort Jian Shou
title Mechanism of increased risk of insulin resistance in aging skeletal muscle
title_short Mechanism of increased risk of insulin resistance in aging skeletal muscle
title_full Mechanism of increased risk of insulin resistance in aging skeletal muscle
title_fullStr Mechanism of increased risk of insulin resistance in aging skeletal muscle
title_full_unstemmed Mechanism of increased risk of insulin resistance in aging skeletal muscle
title_sort mechanism of increased risk of insulin resistance in aging skeletal muscle
publisher BMC
series Diabetology & Metabolic Syndrome
issn 1758-5996
publishDate 2020-02-01
description Abstract As age increases, the risk of developing type 2 diabetes increases, which is associated with senile skeletal muscle dysfunction. During skeletal muscle aging, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, modified activity of insulin sensitivity regulatory enzymes, endoplasmic reticulum stress, decreased autophagy, sarcopenia and over-activated renin-angiotensin system may occur. These changes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during skeletal muscle aging. This review of the mechanism of the increased risk of insulin resistance during skeletal muscle aging will provide a more comprehensive explanation for the increased incidence of type 2 diabetes in elderly individuals, and will also provide a more comprehensive perspective for the prevention and treatment of type 2 diabetes in elderly populations.
topic Skeletal muscle aging
Insulin resistance
Mechanism
url https://doi.org/10.1186/s13098-020-0523-x
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