Hui Li1, Yaoshan Dun2, Wenliang Zhang1, Baiyang You1, Yuan Liu1, Siqian Fu1, Ling Qiu1, Jing Cheng3, Jeffrey W Ripley-Gonzalez1, Suixin Liu4. 1. Division of Cardiac Rehabilitation, Department of Physical Medicine & Rehabilitation, Xiangya Hospital of Central South University, Changsha, Hunan, China. 2. Division of Cardiac Rehabilitation, Department of Physical Medicine & Rehabilitation, Xiangya Hospital of Central South University, Changsha, Hunan, China; Division of Preventive Cardiology, Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, United States. 3. Division of Cardiac Rehabilitation, Department of Cardiovascular Medicine, Shenzhen Yantian People's Hospital, Shenzhen, Guangdong, China. 4. Division of Cardiac Rehabilitation, Department of Physical Medicine & Rehabilitation, Xiangya Hospital of Central South University, Changsha, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital of Central South University, Changsha, Hunan, China.. Electronic address: liusuixin@csu.edu.cn.
Abstract
AIM: To emphasize the mechanism of the effect of exercise on lipid droplet (LD) metabolism disorder in nonalcoholic fatty liver disease (NAFLD). MAIN METHODS: C57BL/6J mice were randomly divided into three groups: The first group was fed with a normal diet (CON), the second group was fed a high-fat diet (HF), and finally group with a high-fat diet intervention and swim training (HF-EX). The total intervention period was 16 weeks. RT-PCR and Western blot were performed to evaluate the effect of exercise on LDs metabolism and the AMPK pathway. Histopathological examinations and immunofluorescence were performed to evaluate the lipid deposition and lipophagy in the liver. KEY FINDINGS: Exercise reduced liver steatosis and insulin resistance along with the stimulation of AMPK/SIRT1 signaling and downstream regulation of lipid metabolism. In addition, exercise increased the expression of autophagy marker and colocalization of LC3 and LAMP1 with LDs. SIGNIFICANCE: Exercise stimulated AMPK/SIRT1 and activated lipophagy in NAFLD. Enhancing lipophagy may be one of the key mechanisms of regulation and resolution of NAFLD by exercise.
AIM: To emphasize the mechanism of the effect of exercise on lipid droplet (LD) metabolism disorder in nonalcoholic fatty liver disease (NAFLD). MAIN METHODS: C57BL/6J mice were randomly divided into three groups: The first group was fed with a normal diet (CON), the second group was fed a high-fat diet (HF), and finally group with a high-fat diet intervention and swim training (HF-EX). The total intervention period was 16 weeks. RT-PCR and Western blot were performed to evaluate the effect of exercise on LDs metabolism and the AMPK pathway. Histopathological examinations and immunofluorescence were performed to evaluate the lipid deposition and lipophagy in the liver. KEY FINDINGS: Exercise reduced liver steatosis and insulin resistance along with the stimulation of AMPK/SIRT1 signaling and downstream regulation of lipid metabolism. In addition, exercise increased the expression of autophagy marker and colocalization of LC3 and LAMP1 with LDs. SIGNIFICANCE: Exercise stimulated AMPK/SIRT1 and activated lipophagy in NAFLD. Enhancing lipophagy may be one of the key mechanisms of regulation and resolution of NAFLD by exercise.
Authors: Robert H Lustig; David Collier; Christopher Kassotis; Troy A Roepke; Min Ji Kim; Etienne Blanc; Robert Barouki; Amita Bansal; Matthew C Cave; Saurabh Chatterjee; Mahua Choudhury; Michael Gilbertson; Dominique Lagadic-Gossmann; Sarah Howard; Lars Lind; Craig R Tomlinson; Jan Vondracek; Jerrold J Heindel Journal: Biochem Pharmacol Date: 2022-04-05 Impact factor: 6.100
Authors: Lifei Liu; Yuhao Liu; Mei Huang; Miao Zhang; Chenyu Zhu; Xi Chen; Samuel Bennett; Jiake Xu; Jun Zou Journal: Front Physiol Date: 2022-07-11 Impact factor: 4.755