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Metabolism. 2016 May;65(5):646-54. doi: 10.1016/j.metabol.2016.01.009. Epub 2016 Jan 25.

Cascade regulation of PPARγ(2) and C/EBPα signaling pathways by celastrol impairs adipocyte differentiation and stimulates lipolysis in 3T3-L1 adipocytes.

Author information

1
Laboratory of Metabolic Engineering, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, South Korea; Institute of Animal Molecular Biotechnology, Korea University, Seoul 02841, South Korea.
2
Mibyeong Research Center, Korea Institute of Oriental Medicine, Daejeon 34054, South Korea.
3
Institute of Animal Molecular Biotechnology, Korea University, Seoul 02841, South Korea; Cell Function Regulation Laboratory, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, South Korea.
4
Mibyeong Research Center, Korea Institute of Oriental Medicine, Daejeon 34054, South Korea. Electronic address: kataz@kiom.re.kr.
5
Laboratory of Metabolic Engineering, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, South Korea; Institute of Animal Molecular Biotechnology, Korea University, Seoul 02841, South Korea; Biomedical Research Center of Guro Hospital, Research Driven Hospital, Korea University, Seoul 08308, South Korea. Electronic address: mhs72@korea.ac.kr.

Abstract

OBJECTIVE:

Celastrol, a triterpene from the root bark of the Chinese medicinal plant Tripterygium wilfordii, has been shown to exhibit anti-oxidant, anti-inflammatory, anti-cancer and insecticidal activities. Also, it has been demonstrated that celastrol has obesity-controlling effects in diet-induced obesity mice. However, direct evidence that celastrol contributes to the development of adipocyte differentiation and lipolysis has not been fully elucidated. Moreover, no previous studies have evaluated whether celastrol may regulate adipogenic transcriptional markers in adipocytes.

MATERIALS/METHODS:

In order to address the questions above, we extended previous observations and investigated in vitro celastrol signaling study whether celastrol may regulate differentiation, lipolysis and key adipogenic transcriptional pathways in 3T3-L1 adipocytes.

RESULTS:

Treatment of celastrol not only inhibited adipocyte differentiation (lipid accumulation, glyceraldehyde-3-phosphate dehydrogenase activity and triglyceride content) but also increased lipolysis (glycerol release and free fatty acid release) in 3T3-L1 adipocytes. In addition, all celastrol-regulated functional activities were controlled by PPARγ(2) and C/EBPα signaling pathways in duration of celastrol's treatment in 3T3-L1 adipocytes.

CONCLUSION:

Our initial data from in vitro celastrol signaling studies suggest novel insights into the role of PPARγ(2) and C/EBPα as probable mediators of the action of celastrol in regulating adipocyte differentiation and lipolysis in 3T3-L1 adipocytes.

KEYWORDS:

Adipocytes differentiation; C/EBPα; Celastrol; Lipolysis; PPARγ(2)

PMID:
27085773
DOI:
10.1016/j.metabol.2016.01.009
[Indexed for MEDLINE]

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