Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice.
Physical exercise is an important and effective therapy for diabetes. However, its underlying mechanism is not fully understood. Protein kinase Cβ (PKCβ) has been suggested to be involved in the pathogenesis of obesity and insulin resistance, but the role of PKCβ in exercise-induced improvements in...
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doaj-51a26331d44b4e299051b1ccee77798f2020-11-25T02:29:05ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-01812e8136410.1371/journal.pone.0081364Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice.Xiaoquan RaoJixin ZhongXiaohua XuBrianna JordanSantosh MauryaZachary BraunsteinTse-Yao WangWei HuangSudha AggarwalMuthu PeriasamySanjay RajagopalanKamal MehtaQinghua SunPhysical exercise is an important and effective therapy for diabetes. However, its underlying mechanism is not fully understood. Protein kinase Cβ (PKCβ) has been suggested to be involved in the pathogenesis of obesity and insulin resistance, but the role of PKCβ in exercise-induced improvements in insulin resistance is completely unknown. In this study, we evaluated the involvement of PKCβ in exercise-attenuated insulin resistance in high-fat diet (HFD)-fed mice. PKCβ(-/-) and wild-type mice were fed a HFD with or without exercise training. PKC protein expression, body and tissue weight change, glucose and insulin tolerance, metabolic rate, mitochondria size and number, adipose inflammation, and AKT activation were determined to evaluate insulin sensitivity and metabolic changes after intervention. PKCβ expression decreased in both skeletal muscle and liver tissue after exercise. Exercise and PKCβ deficiency can alleviate HFD-induced insulin resistance, as evidenced by improved insulin tolerance. In addition, fat accumulation and mitochondrial dysfunction induced by HFD were also ameliorated by both exercise and PKCβ deficiency. On the other hand, exercise had little effect on PKCβ(-/-) mice. Further, our data indicated improved activation of AKT, the downstream signal molecule of insulin, in skeletal muscle and liver of exercised mice, whereas PKCβ deficiency blunted the difference between sedentary and exercised mice. These results suggest that downregulation of PKCβ contributes to exercise-induced improvement of insulin resistance in HFD-fed mice.http://europepmc.org/articles/PMC3857188?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Xiaoquan Rao Jixin Zhong Xiaohua Xu Brianna Jordan Santosh Maurya Zachary Braunstein Tse-Yao Wang Wei Huang Sudha Aggarwal Muthu Periasamy Sanjay Rajagopalan Kamal Mehta Qinghua Sun |
spellingShingle |
Xiaoquan Rao Jixin Zhong Xiaohua Xu Brianna Jordan Santosh Maurya Zachary Braunstein Tse-Yao Wang Wei Huang Sudha Aggarwal Muthu Periasamy Sanjay Rajagopalan Kamal Mehta Qinghua Sun Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice. PLoS ONE |
author_facet |
Xiaoquan Rao Jixin Zhong Xiaohua Xu Brianna Jordan Santosh Maurya Zachary Braunstein Tse-Yao Wang Wei Huang Sudha Aggarwal Muthu Periasamy Sanjay Rajagopalan Kamal Mehta Qinghua Sun |
author_sort |
Xiaoquan Rao |
title |
Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice. |
title_short |
Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice. |
title_full |
Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice. |
title_fullStr |
Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice. |
title_full_unstemmed |
Exercise protects against diet-induced insulin resistance through downregulation of protein kinase Cβ in mice. |
title_sort |
exercise protects against diet-induced insulin resistance through downregulation of protein kinase cβ in mice. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2013-01-01 |
description |
Physical exercise is an important and effective therapy for diabetes. However, its underlying mechanism is not fully understood. Protein kinase Cβ (PKCβ) has been suggested to be involved in the pathogenesis of obesity and insulin resistance, but the role of PKCβ in exercise-induced improvements in insulin resistance is completely unknown. In this study, we evaluated the involvement of PKCβ in exercise-attenuated insulin resistance in high-fat diet (HFD)-fed mice. PKCβ(-/-) and wild-type mice were fed a HFD with or without exercise training. PKC protein expression, body and tissue weight change, glucose and insulin tolerance, metabolic rate, mitochondria size and number, adipose inflammation, and AKT activation were determined to evaluate insulin sensitivity and metabolic changes after intervention. PKCβ expression decreased in both skeletal muscle and liver tissue after exercise. Exercise and PKCβ deficiency can alleviate HFD-induced insulin resistance, as evidenced by improved insulin tolerance. In addition, fat accumulation and mitochondrial dysfunction induced by HFD were also ameliorated by both exercise and PKCβ deficiency. On the other hand, exercise had little effect on PKCβ(-/-) mice. Further, our data indicated improved activation of AKT, the downstream signal molecule of insulin, in skeletal muscle and liver of exercised mice, whereas PKCβ deficiency blunted the difference between sedentary and exercised mice. These results suggest that downregulation of PKCβ contributes to exercise-induced improvement of insulin resistance in HFD-fed mice. |
url |
http://europepmc.org/articles/PMC3857188?pdf=render |
work_keys_str_mv |
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