Research Paper Volume 11, Issue 8 pp 2217—2240

Resveratrol prevents sarcopenic obesity by reversing mitochondrial dysfunction and oxidative stress via the PKA/LKB1/AMPK pathway

Yujie Huang1, , Xiaohui Zhu1, , Ka Chen1, , Hedong Lang1, , Yong Zhang1, , Pengfei Hou1, , Li Ran1, , Min Zhou1, , Jiawei Zheng1, , Long Yi1, , Mantian Mi1, , Qianyong Zhang1, ,

  • 1 Research Center for Nutrition and Food Safety, Chongqing Key Laboratory of Nutrition and Food Safety, Institute of Military Preventive Medicine, Third Military Medical University, Shapingba District, Chongqing 400038, P. R. China

Received: November 15, 2018       Accepted: April 4, 2019       Published: April 15, 2019
How to Cite

Copyright: Huang et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Background: The concept of sarcopenic obesity refers to low muscle mass coupled with high adiposity in older adults. Sarcopenic obesity is a new medical challenge that imposes tremendous financial burdens on healthcare authorities worldwide. This study investigated the effects of resveratrol on high-fat diet-induced sarcopenic obesity in aged rats and palmitate acid-induced muscle atrophy in L6 myotubes and explored the underlying mechanisms.

Results: In vivo, resveratrol prevented muscle loss and myofiber size decrease, improved grip strength and abolished excessive fat accumulation. In vitro, resveratrol inhibited the palmitate acid-mediated reductions in myosin heavy chain content and myotube diameter. Moreover, resveratrol ameliorated mitochondrial dysfunction and oxidative stress, leading to an improvement in protein metabolism and contributing to the prevention of muscle atrophy. Furthermore, the protective effects of resveratrol on mitochondrial function, oxidative stress and muscle atrophy were abolished by PKA siRNA, LKB1 siRNA and AMPK siRNA transfection in vitro.

Conclusions: Resveratrol prevented high-fat diet-induced muscle atrophy in aged rats by reversing mitochondrial dysfunction and oxidative stress, which was partially mediated by the PKA/LKB1/AMPK pathway. These findings indicate that resveratrol might have potential uses for the prevention and treatment of sarcopenic obesity.


PKA: protein kinase A; LKB1: liver kinase B1; AMPK: AMP-activated protein kinase; CD: chow diet; HFD: high fat diet; PA: palmitate acid; RSV: resveratrol; CCK-8: Cell Counting Kit-8; TG: total triglyceride; TC: total cholesterol; HDL-C: high-density lipoprotein cholesterol; LDL-C: low-density lipoprotein cholesterol; VAT: visceral adipose tissue; SAT: subcutaneous adipose tissue; IFM: intermyofibrillar mitochondria; SSM: subsarcolemmal mitochondria; TEM: transmission electron microscopy; Δψm: mitochondrial membrane potential; OCR: oxygen consumption rate; ROS: reactive oxygen species; mtROS: mitochondrial ROS; T-AOC: total antioxidative capability; SOD: superoxide dismutase; GPx: glutathione peroxidase; MDA: malonaldehyde; NAC: N-acetyl-L-cysteine; MHC: myosin heavy chain.