title: Endoplasmic reticulum stress suppresses lipin-1 expression in 3T3-L1 adipocytes.
abstract: 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.
authors.affiliation: Department of Internal Medicine, School of Dentistry, Health Sciences University of Hokkaido, 1757, Kanazawa, Ishikari-Toubetsu, Hokkaido 061-0023, Japan. ntkhs@hoku-iryo-u.ac.jp
authors.forename: Nobuhiko
authors.initials: N
authors.lastname: Takahashi
authors.forename: Takayuki
authors.initials: T
authors.lastname: Yoshizaki
authors.forename: Natsumi
authors.initials: N
authors.lastname: Hiranaka
authors.forename: Takeshi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Tomoo
authors.initials: T
authors.lastname: Yui
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Akanuma
authors.forename: Kaoru
authors.initials: K
authors.lastname: Kanazawa
authors.forename: Mika
authors.initials: M
authors.lastname: Yoshida
authors.forename: Sumiyoshi
authors.initials: S
authors.lastname: Naito
authors.forename: Mikihiro
authors.initials: M
authors.lastname: Fujiya
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kohgo
authors.forename: Masahiro
authors.initials: M
authors.lastname: Ieko
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D009687:Nuclear Proteins / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D047495:PPAR gamma / Q000819:agonists / Q000378:metabolism; D010711:Phosphatidate Phosphatase / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000235:genetics; D019284:Thapsigargin / Q000494:pharmacology; D014158:Transcription, Genetic / Q000187:drug effects; D014415:Tunicamycin / Q000494:pharmacology
chemical_list: D009687:Nuclear Proteins; D047495:PPAR gamma; D014415:Tunicamycin; D019284:Thapsigargin; C418978:Lpin1 protein, mouse; D010711:Phosphatidate Phosphatase