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Suppression of Adipocyte Differentiation by Foenumoside B from Lysimachia foenum-graecum Is Mediated by PPAR. Antagonismopen access

Authors
Kwak, Hyun JeongChoi, Hye-EunJang, JinsunPark, Soo KyoungCho, Byoung HeonKim, Seul KiLee, SunyiKang, Nam SookCheon, Hyae Gyeong
Issue Date
May-2016
Publisher
PUBLIC LIBRARY SCIENCE
Citation
PLOS ONE, v.11, no.5
Journal Title
PLOS ONE
Volume
11
Number
5
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/9825
DOI
10.1371/journal.pone.0155432
ISSN
1932-6203
Abstract
Lysimachia foenum-graecum extract (LFE) and its active component foenumoside B (FSB) have been shown to inhibit adipocyte differentiation, but their mechanisms were poorly defined. Here, we investigated the molecular mechanisms responsible for their anti-adipogenic effects. Both LFE and FSB inhibited the differentiation of 3T3-L1 preadipocytes induced by peroxisome proliferator-activated receptor-gamma (PPAR gamma) agonists, accompanied by reductions in the expressions of the lipogenic genes aP2, CD36, and FAS. Moreover, LFE and FSB inhibited PPAR gamma transactivation activity with IC(50)s of 22.5 mu g/ml and 7.63 mu g/ml, respectively, and showed selectivity against PPAR alpha and PPAR delta. Rosiglitazone-induced interaction between PPAR. ligand binding domain (LBD) and coactivator SRC-1 was blocked by LFE or FSB, whereas reduced NCoR-1 binding to PPAR gamma by rosiglitazone was reversed in the presence of LFE or FSB. In vivo administration of LFE into either ob/ob mice or KKAy mice reduced body weights, and levels of PPAR gamma and C/EBP alpha in fat tissues. Furthermore, insulin resistance was ameliorated by LFE treatment, with reduced adipose tissue inflammation and hepatic steatosis. Thus, LFE and FSB were found to act as PPAR gamma antagonists that improve insulin sensitivity and metabolic profiles. We propose that LFE and its active component FSB offer a new therapeutic strategy for metabolic disorders including obesity and insulin resistance.
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