Int J Biol Sci 2021; 17(12):3173-3187. doi:10.7150/ijbs.62556 This issue
1. Department of Clinical Nutrition, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
2. College of Basic Medical Science, Institute of Translational Medicine, Key Laboratory of Medical Cell Biology, Ministry of Education, Key Laboratory of Liaoning Province, China Medical University, Shenyang, Liaoning Province, P.R. China, 110122.
3. Institute of Health Sciences, China Medical University, Shenyang 110122, Liaoning, China
4. The VIP Department, School and Hospital of Stomatology, China Medical University, Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang, 110002, China.
5. Department of Radiation Oncology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China.
Pharmacological stimulation of adipose tissue remodeling and thermogenesis to increase energy expenditure is expected to be a viable therapeutic strategy for obesity. Berberine has been reported to have pharmacological activity in adipose tissue to anti-obesity, while the mechanism remains unclear. Here, we observed that berberine significantly reduced the body weight and insulin resistance of high-fat diet mice by promoting the distribution of brown adipose tissue and thermogenesis. We have further demonstrated that berberine activated energy metabolic sensing pathway AMPK/SIRT1 axis to increase the level of PPARγ deacetylation, which leads to promoting adipose tissue remodeling and increasing the expression of the thermogenic protein UCP-1. These findings suggest that berberine that enhances the AMPK/SIRT1 pathway can act as a selective PPARγ activator to promote adipose tissue remodeling and thermogenesis. This study proposes a new mechanism for the regulation of berberine in adipose tissue and offers a great prospect for berberine in obesity treatment
Keywords: Berberine, Adipose tissue, Deacetylation, PPARγ, AMPK/SIRT1 axis