Regulation of adipocyte differentiation by histone deacetylase inhibitors

Authors
Kim, Su-NamChoi, Hye-YoungKim, Yong Kee
Issue Date
2009-04
Publisher
PHARMACEUTICAL SOC KOREA
Citation
ARCHIVES OF PHARMACAL RESEARCH, v.32, no.4, pp.535 - 541
Abstract
In this study, we investigated the effects of various histone deacetylase (HDAC) inhibitors on adipocyte differentiation. Treatment of 3T3-L1 cells with HDAC inhibitors such as apicidin, trichostatin A, or suberoylanilide hydroxamic acid, under conditions that normally promote differentiation led to a dramatic attenuation of adipocyte differentiation. In contrast, sodium butyrate (NaB) treatment increased adipocyte differentiation. Accordingly, the expression of adipogenic marker genes such as FAS, aP2, PPAR gamma, resistin, C/EBP alpha, ADD1/SREBP1c, and adiponectin were inhibited by apicidin treatment but not NaB, indicating that the adipocyte differentiation process could be differentially regulated depending on the type of HDAC inhibitor utilized. In addition, this differential effect seemed not to be due to disruption of the insulin- signaling pathway. Interestingly, our data showed that apicidin treatment could induce dedifferentiation of fully differentiated adipocytes, as evident by the fact that apicidin treatment led to a decrease of Oil Red O-stained adipocytes with a concomitant reduction in the expression levels of adipogenic marker genes. Collectively, our results suggest that adipocyte differentiation and dedifferentiation may be regulated by HDAC inhibitors.
Keywords
SP1 SITES; TRANSCRIPTIONAL REGULATION; EXPRESSION; APICIDIN; RECEPTOR; PROTEIN; KINASE; ADIPOGENESIS; ACTIVATION; PATHWAYS; SP1 SITES; TRANSCRIPTIONAL REGULATION; EXPRESSION; APICIDIN; RECEPTOR; PROTEIN; KINASE; ADIPOGENESIS; ACTIVATION; PATHWAYS; Adipocyte differentiation; Dedifferentiation; HDAC inhibitors; Apicidin; NaB
ISSN
0253-6269
URI
https://pubs.kist.re.kr/handle/201004/132613
DOI
10.1007/s12272-009-1409-5
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KIST Article > 2009
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