Baicalin attenuates diet-induced obesity partially through promoting thermogenesis in adipose tissue
- PMID: 34465552
- DOI: 10.1016/j.orcp.2021.08.003
Baicalin attenuates diet-induced obesity partially through promoting thermogenesis in adipose tissue
Abstract
Background: Adipose tissues have essential roles on energy homeostasis and the development of metabolic syndrome and obesity, they have become critical targets for treating obesity and metabolic disorders. Baicalin is a flavonoid that derived from the root of Scutellaria baicalensis, and it has been reported to take part in the regulation of adipocyte function. All these highlighted the potential of baicalin in the regulation of fat accumulation and obesity. Yet the impact of baicalin on thermogenic function of adipocytes remains to be deciphered.
Objective: This study aims to explore the anti-obesity effects of baicalin.
Materials & methods: The level of mRNA was detected by qRT-PCR and the protein expression level was examined by western blot. H&E staining was used for the observation of the structure of adipose tissue. Serum triglyceride and insulin levels were detected by commercial test kits.
Results: Our data demonstrated that baicalin up-regulates the expression of UCP1 and PGC1a in a dose-dependent manner in vitro. Baicalin also increases ERK phosphorylation, and the increased expression of UCP1 and PGC1a in adipocytes could be inhibited by an ERK inhibitor, U0126. Moreover, dietary baicalin ameliorates high fat diet (HFD)-induced obesity without affecting food intake. In addition, dietary baicalin inhibits adipocyte hypertrophy and enhances thermogenic gene program in sWAT and intrascapular brown adipose tissue (iBAT) in vivo.
Discussion & conclusion: Baicalin prevents HFD-induced obesity partially through promoting adipocyte thermogenesis. Baicalin may be a promising compound against human obesity and related metabolic diseases.
Keywords: Baicalin; Beige adipocytes; Obesity; Subcutaneous WAT; Thermogenesis; UCP1; WAT browning.
Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.
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