scholarly journals Celastrol prevents high‐fat diet‐induced obesity by promoting white adipose tissue browning

2021 ◽  
Vol 11 (12) ◽  
Author(s):  
Bingwei Wang ◽  
Xiaoning Yang ◽  
Miao Zhao ◽  
Zhijie Su ◽  
Zhiping Hu ◽  
...  
2021 ◽  
Author(s):  
Xiao Guo ◽  
Xuedan Cao ◽  
Xiugui Fang ◽  
Ailing Guo ◽  
Erhu Li

In this study, Ougan juice (OJ) and lactic acid bacteria fermented Ougan juice (FOJ) were investigated individually for their capability of preventing obesity in high-fat diet (HFD)-fed C57BL/6J mice. After...


Planta Medica ◽  
2012 ◽  
Vol 78 (10) ◽  
pp. 943-950 ◽  
Author(s):  
Thing-Fong Tzeng ◽  
Hung-Jen Lu ◽  
Shorong-Shii Liou ◽  
Chia Chang ◽  
I-Min Liu

Endocrinology ◽  
2015 ◽  
Vol 156 (1) ◽  
pp. 147-156 ◽  
Author(s):  
Jung-Hwan Baek ◽  
Seok-Jun Kim ◽  
Hyeok Gu Kang ◽  
Hyun-Woo Lee ◽  
Jung-Hoon Kim ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jessica E. C. Jones ◽  
Nabil Rabhi ◽  
Joseph Orofino ◽  
Ramya Gamini ◽  
Valentina Perissi ◽  
...  

AbstractVisceral white adipose tissue (vWAT) expands and undergoes extensive remodeling during diet-induced obesity. Much is known about the contribution of various stromal vascular cells to the remodeling process, but less is known of the changes that occur within the adipocyte as it becomes progressively dysfunctional. Here, we performed a transcriptome analysis of isolated vWAT adipocytes to assess global pathway changes occurring in response to a chronic high fat diet (HFD). The data demonstrate that the adipocyte responds to the HFD by adopting a fibroblast-like phenotype, characterized by enhanced expression of ECM, focal adhesion and cytoskeletal genes and suppression of many adipocyte programs most notably those associated with mitochondria. This study reveals that during obesity the adipocyte progressively becomes metabolically dysfunctional due to its acquisition of fibrogenic functions. We propose that mechano-responsive transcription factors such as MRTFA and SRF contribute to both upregulation of morphological genes as well as suppression of mitochondrial programs.


2012 ◽  
Vol 258 (1) ◽  
pp. 32-42 ◽  
Author(s):  
Takashige Kawakami ◽  
Norihide Hanao ◽  
Kaori Nishiyama ◽  
Yoshito Kadota ◽  
Masahisa Inoue ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhuohui Luo ◽  
Jiawen Huang ◽  
Zhiping Li ◽  
Zhiwen Liu ◽  
Linchun Fu ◽  
...  

Cajanolactone A (CLA) is a stilbenoid isolated from Cajanus canjan (L.) Millsp with the potential to prevent postmenopausal obesity. In this study, the effect of CLA on high-fat diet (HFD)-induced obesity in female C57BL/6 mice was investigated. It was found that, treatment with CLA reduced the energy intake and effectively protected the mice from HFD-induced body weight gain, fat accumulation within the adipose tissues and liver, and impairment in energy metabolism. Further investigation revealed that CLA significantly down-regulated the expression of ORX, ORXR2, pMCH, and Gal in the hypothalamus and antagonized HFD-induced changes in the expression of UCP1, Pgc-1α, Tfam, and Mfn1 in the inguinal white adipose tissue (iWAT); Caveolin-1, MT and UCP3 in the perigonadal white adipose tissue (pWAT); and Pdhb, IRS2, Mttp, Hadhb, and Cpt1b in the liver. CLA also protected the pWAT and liver from HFD-induced mitochondrial damage. However, neither HFD nor CLA showed an effect on the mass of brown adipose tissue (BAT) or the expression of UCP1 in the BAT. In summary, our findings suggest that CLA is a potential drug candidate for preventing diet-induced obesity, at least in females. CLA works most likely by suppressing the hypothalamic expression of orexigenic genes, which leads to reduced energy intake, and subsequently, reduced fat accumulation, thereby protecting the adipose tissues and the liver from lipid-induced mitochondrial dysfunction.


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