Cascade regulation of PPARγ2 and C/EBPα signaling pathways by celastrol impairs adipocyte differentiation and stimulates lipolysis in 3T3-L1 adipocytes

Seung Kug Choi, Sunmi Park, Subin Jang, Hun Hee Cho, Siwoo Lee, Seungkwon You, Sang Hyuk Kim, Hyun-Seuk Moon

Research output: Contribution to journalArticle

20 Citations (Scopus)

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 PPARγ2 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 PPARγ2 and C/EBPα as probable mediators of the action of celastrol in regulating adipocyte differentiation and lipolysis in 3T3-L1 adipocytes.

Original languageEnglish
Pages (from-to)646-654
Number of pages9
JournalMetabolism: Clinical and Experimental
Volume65
Issue number5
DOIs
Publication statusPublished - 2016 May 1

Fingerprint

Lipolysis
Adipocytes
tripterine
Obesity
Tripterygium
Triterpenes
Glyceraldehyde-3-Phosphate Dehydrogenases
Medicinal Plants
Nonesterified Fatty Acids
Oxidants
Glycerol
Triglycerides
Anti-Inflammatory Agents
Diet
Lipids

Keywords

  • Adipocytes differentiation
  • C/EBPα
  • Celastrol
  • Lipolysis
  • PPARγ

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Cascade regulation of PPARγ2 and C/EBPα signaling pathways by celastrol impairs adipocyte differentiation and stimulates lipolysis in 3T3-L1 adipocytes. / Choi, Seung Kug; Park, Sunmi; Jang, Subin; Cho, Hun Hee; Lee, Siwoo; You, Seungkwon; Kim, Sang Hyuk; Moon, Hyun-Seuk.

In: Metabolism: Clinical and Experimental, Vol. 65, No. 5, 01.05.2016, p. 646-654.

Research output: Contribution to journalArticle

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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 PPARγ2 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 PPARγ2 and C/EBPα as probable mediators of the action of celastrol in regulating adipocyte differentiation and lipolysis in 3T3-L1 adipocytes.",
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T1 - Cascade regulation of PPARγ2 and C/EBPα signaling pathways by celastrol impairs adipocyte differentiation and stimulates lipolysis in 3T3-L1 adipocytes

AU - Choi, Seung Kug

AU - Park, Sunmi

AU - Jang, Subin

AU - Cho, Hun Hee

AU - Lee, Siwoo

AU - You, Seungkwon

AU - Kim, Sang Hyuk

AU - Moon, Hyun-Seuk

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N2 - 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 PPARγ2 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 PPARγ2 and C/EBPα as probable mediators of the action of celastrol in regulating adipocyte differentiation and lipolysis in 3T3-L1 adipocytes.

AB - 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 PPARγ2 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 PPARγ2 and C/EBPα as probable mediators of the action of celastrol in regulating adipocyte differentiation and lipolysis in 3T3-L1 adipocytes.

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