Endoplasmic reticulum stress suppresses lipin-1 expression in 3T3-L1 adipocytes
著者
高橋, 伸彦
(Takahashi, Nobuhiko)
Yoshizaki, Takayuki
Hiranaka, Natsumi
Suzuki, Takeshi
Yui, Tomoo
Akanuma, Masayasu
Kanazawa, Kaoru
Yoshida, Mika
Naito, Sumiyoshi
藤谷, 幹浩
(Fujiya, Mikihiro)
高後, 裕
(Kohgo, Yutaka)
Ieko, Masahiro
上位タイトル
Biochemical and biophysical research communications
Vol.431,
No.1
(2013.
2)
,p.25-
30
識別番号
ISSN
0006-291X
DOI
10.1016/j.bbrc.2012.12.112
その他
PMID：23291236
抄録
Lipin-1 plays crucial roles in the regulation of lipid metabolism and cell differentiation in adipocytes. In obesity, adipose lipin-1 mRNA expression is decreased and positively correlated with systemic insulin sensitivity. Amelioration of the lipin-1 depletion might be improved dysmetabolism. Although some cytokines such as TNF-α and interleukin-1β reduces adipose lipin-1 expression, the mechanism of decreased adipose lipin-1 expression in obesity remains unclear. Recently, endoplasmic reticulum (ER) stress is implicated in the pathogenesis of obesity. Here we investigated the role of ER stress on the lipin-1 expression in 3T3-L1 adipocytes. We demonstrated that lipin-1 expression was suppressed by the treatment with ER stress inducers (tunicamycin and thapsigargin) at transcriptional level. We also showed that constitutive lipin-1 expression could be maintained by peroxisome proliferator-activated receptor-γ in 3T3-L1 adipocytes. Activation of peroxisome proliferator-activated receptor-γ recovered the ER stress-induced lipin-1 suppression. These results suggested that ER stress might be involved in the pathogenesis of obesity through lipin-1 depletion.
