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Exp Clin Endocrinol Diabetes 2017; 125(08): 538-546
DOI: 10.1055/s-0043-104634
Article
© Georg Thieme Verlag KG Stuttgart · New York

Early Mitochondrial Adaptations in Skeletal Muscle to Obesity and Obesity Resistance Differentially Regulated by High-Fat Diet

Jingyu Sun
1   Sports and Health Research Center, Tongji University Department of Physical Education, Shanghai, China
,
Tao Huang
2   Department of Physical Education, Shanghai Jiao Tong University, Shanghai, China
,
Zhengtang Qi
3   Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai, China
,
Songhui You
1   Sports and Health Research Center, Tongji University Department of Physical Education, Shanghai, China
,
Jingmei Dong
1   Sports and Health Research Center, Tongji University Department of Physical Education, Shanghai, China
,
Chen Zhang
4   Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China
,
Lili Qin
1   Sports and Health Research Center, Tongji University Department of Physical Education, Shanghai, China
,
Yunhe Zhou
1   Sports and Health Research Center, Tongji University Department of Physical Education, Shanghai, China
,
Shuzhe Ding
3   Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai, China
› Author Affiliations
Further Information

Publication History

received 21 October 2016
revised 17 February 2017

accepted 23 February 2017

Publication Date:
25 April 2017 (online)

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Abstract

Objective

The mechanism for different susceptibilities to obesity after short-term high-fat diet (HFD) feeding is largely unknown. Given the close association between obesity occurrence and mitochondrial dysfunction, the early events in skeletal muscle mitochondrial adaptations between HFD-induced obesity (DIO) and HFD-induced obesity resistant (DIO-R) lean phenotype under excess nutritional environment were explored.

Methods

ICR/JCL male mice were randomly divided into 2 groups, as follows: low-fat diet (LFD) and HFD groups. After 6 weeks on HFD, HFD-fed mice were classified as DIO or DIO-R according to their body weight gain. Serum parameters, oxidative stress biomarkers, the activation of AMPK/ACC axis, and the expression profiles of mitochondrial biogenesis were measured by using corresponding methods among the LFD control, DIO, and DIO-R groups.

Results

Serum glucose, total cholesterol, low-density lipoprotein, and high-density lipoprotein levels were significantly increased in DIO and DIO-R mice compared with LFD controls. However, DIO-R mice had significantly higher MDA levels and exhibited a significantly higher level of AMP-activated protein kinase (AMPK) activation and acetyl-CoA carboxylase (ACC) inactivation than DIO mice. Furthermore, the transcript and protein levels of transcriptional coactivator peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α (PGC-1α) and estrogen-related receptor-α (ERRα) in DIO-R mice were significantly up-regulated compared with the DIO mice.

Conclusions

Although the body weight gain differed, the DIO and DIO-R mice had similar metabolic disturbance of glucose and lipids after short-term HFD consumption. The diverse alterations on fatty acid oxidation and mitochondrial biogenesis pathway induced by AMPK activation might be involved in different susceptibilities to obesity when consuming HFD.

Key words

high-fat diet-induced obesity - high-fat diet-induced obesity resistance - fatty acid oxidation - mitochondrial biogenesis
 

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