論文

国際誌
2020年3月27日

CREBH Improves Diet-Induced Obesity, Insulin Resistance, and Metabolic Disturbances by FGF21-Dependent and FGF21-Independent Mechanisms.

iScience
  • Aoi Satoh
  • ,
  • Song-Iee Han
  • ,
  • Masaya Araki
  • ,
  • Yoshimi Nakagawa
  • ,
  • Hiroshi Ohno
  • ,
  • Yuhei Mizunoe
  • ,
  • Kae Kumagai
  • ,
  • Yuki Murayama
  • ,
  • Yoshinori Osaki
  • ,
  • Hitoshi Iwasaki
  • ,
  • Motohiro Sekiya
  • ,
  • Morichika Konishi
  • ,
  • Nobuyuki Itoh
  • ,
  • Takashi Matsuzaka
  • ,
  • Hirohito Sone
  • ,
  • Hitoshi Shimano

23
3
開始ページ
100930
終了ページ
100930
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.isci.2020.100930

Mice overexpressing the nuclear form of CREBH mainly in the liver (CREBH-Tg) showed suppression of high-fat high-sucrose (HFHS) diet-induced obesity accompanied by an increase in plasma fibroblast growth factor 21 (FGF21) levels. CREBH overexpression induced browning in inguinal white adipose tissue (WAT) and whole-body energy expenditure, which was canceled in Fgf21-/- mice. Deficiency of FGF21 in CREBH-Tg mice mostly canceled the improvement of obesity, but the suppression of inflammation of epidermal WAT, amelioration of insulin resistance, and improvement of glucose metabolism still sustained. Kisspeptin 1 (Kiss1) was identified as a novel hormone target for CREBH to explain these FGF21-independent effects of CREBH. Knockdown of Kiss1 in HFHS-fed CREBH-Tg Fgf21-/- mice showed partially canceled improvement of glucose metabolism. Taken together, we propose that hepatic CREBH pleiotropically improves diet-induced obesity-mediated dysfunctions in peripheral tissues by improving systemic energy metabolism in FGF21-dependent and FGF21-independent mechanisms.

リンク情報
DOI
https://doi.org/10.1016/j.isci.2020.100930
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32151974
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063134
ID情報
  • DOI : 10.1016/j.isci.2020.100930
  • PubMed ID : 32151974
  • PubMed Central 記事ID : PMC7063134

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