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Electroacupuncture Regulates Inguinal White Adipose Tissue Browning by Promoting Sirtuin-1-Dependent PPAR γ Deacetylation and Mitochondrial Biogenesis.

Authors :
Tang Q
Lu M
Xu B
Wang Y
Lu S
Yu Z
Jing X
Yuan J
Source :
Frontiers in endocrinology [Front Endocrinol (Lausanne)] 2021 Jan 21; Vol. 11, pp. 607113. Date of Electronic Publication: 2021 Jan 21 (Print Publication: 2020).
Publication Year :
2021

Abstract

Background: Previous studies had suggested that electroacupuncture (EA) can promote white adipose tissue (WAT) browning to counter obesity. But the mechanism was still not very clear.<br />Aim: In this study, we aim to study the effect of EA on promoting inguinal WAT (iWAT) browning and its possible mechanism.<br />Method: Three-week-old rats were randomly divided into a normal diet (ND) group and a high-fat diet (HFD) group. After 10 weeks, the HFD rats were grouped into HFD + EA group and HFD control group. Rats in the EA group were electro-acupunctured for 4 weeks on Tianshu (ST25) acupoint under gas anesthesia with isoflurane, while the rats in HFD group were under gas anesthesia only. Body weight and cumulative food intake were monitored, and H&E staining was performed to assess adipocyte area. The effect of EA on WAT was assessed by qPCR, immunoblotting, immunoprecipitation and Co-immunoprecipitation. Mitochondria were isolated from IWAT to observe the expression of mitochondrial transcription factor A (TFAM).<br />Results: The body weight, WAT/body weight ratio and cumulative food consumption obviously decreased (P < 0.05) in the EA group. The expressions of brown adipose tissue (BAT) markers were increased in the iWAT of EA rats. Nevertheless, the mRNA expressions of WAT genes were suppressed by 4-week EA treatment. Moreover, EA increased the protein expressions of SIRT-1, PPAR γ , PGC-1 α , UCP1 and PRDM16 which trigger the molecular conversion of iWAT browning. The decrease of PPAR γ acetylation was also found in EA group, indicating EA could advance WAT-browning through SIRT-1 dependent PPAR γ deacetylation pathway. Besides, we found that EA could activate AMPK to further regulate PGC-1 α -TFAM-UCP1 pathway to induce mitochondrial biogenesis.<br />Conclusion: In conclusion, EA can remodel WAT to BAT through inducing SIRT-1 dependent PPAR γ deacetylation, and regulating PGC-1 α -TFAM-UCP1 pathway to induce mitochondrial biogenesis. This may be one of the mechanisms by which EA affects weight loss.<br />Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2021 Tang, Lu, Xu, Wang, Lu, Yu, Jing and Yuan.)

Details

Language :
English
ISSN :
1664-2392
Volume :
11
Database :
MEDLINE
Journal :
Frontiers in endocrinology
Publication Type :
Academic Journal
Accession number :
33551999
Full Text :
https://doi.org/10.3389/fendo.2020.607113