Abstract

The extract of the Gardenia jasminoides fruit (GJFE) can been consumed as an herbal tea or used as a yellow dye. Recently, studies report that GFJE exerts inhibitory effects on lipid accumulation and adipogenesis in white adipocytes. We evaluated the thermogenic actions of GJFE by focusing on mitochondrial activation and studying the underlying mechanisms. To investigate the role of GJFE on thermogenesis in mice, we used an acute cold exposure model. After 2 weeks of feeding, the cold tolerance of GJFE-fed mice was notably increased compared to PBS-fed mice. This was due to an increase in thermogenic proteins in the inguinal white adipose tissue of the cold-exposed mice. Moreover, GJFE significantly increased thermogenic factors such as peroxisome proliferator-activated receptor gamma (PPARγ), uncoupling protein 1 (UCP1), and PPARγ coactivator 1 alpha (PGC1α) in vitro as well. Factors related to mitochondrial abundance and functions were also induced by GJFE in white and beige adipocytes. However, the treatment of PPARγ inhibitor abolished the GJFE-induced changes, indicating that activation of PPARγ is critical for the thermogenic effect of GJFE. In conclusion, GJFE induces thermogenic action by activating mitochondrial function via PPARγ activation. Through these findings, we suggest GJFE as a potential anti-obesity agent with a novel mechanism involving thermogenic action in white adipocytes.

Highlights

  • The rectal temperature of the PBS-fed mice decreased to 30.1 ± 1.6 ◦ C but that of the GJFE-fed mice was relatively stable at 34.6 ± 0.5 ◦ C (Figure 1A)

  • The cold exposure seemed to reduce the amount of inguinal white adipose tissue (iWAT), epididymal white adipose tissue (eWAT), and brown adipose tissue (BAT) in both the PBS- and GJFE-treated mice (Figure S2B)

  • The adipose tissues were stained with Hematoxylin and Eosin (H&E) to visualize the morphological change in the lipid droplets of the adipose tissues

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Summary

Introduction

Obesity is a major health threat worldwide and a risk factor of various fatal diseases including type 2 diabetes, cardiovascular diseases, and even cancer [1]. The global incidence of obesity is rapidly increasing [2]. The imbalance between energy intake and expenditure is the main cause of obesity. The contribution of brown adipose tissue (BAT) to energy expenditure has been widely accepted since its unexpected rediscovery in 2007 [3]. White adipose tissue (WAT) stores excess energy as triglycerides; BAT induces uncoupled mitochondrial

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