Glucocorticoids increase NPY gene expression in the arcuate nucleus by inhibiting mTOR signaling in rat hypothalamic organotypic cultures

Hiroshi Shimizu, Hiroshi Arima, Yoshiharu Ozawa, Minemori Watanabe, Ryoichi Banno, Yoshihisa Sugimura, Nobuaki Ozaki, Hiroshi Nagasaki, Yutaka Oiso

研究成果: Article査読

26 被引用数 (Scopus)

抄録

The mammalian target of rapamycin (mTOR) has been implicated in the regulation of physiological functions such as cell growth and proliferation, and glucocorticoids reportedly inhibit mTOR signaling in peripheral tissues. Recent studies suggest that the mTOR signaling in the hypothalamus plays a critical role in maintaining energy homeostasis. In this study, we examined whether the mTOR signaling in the hypothalamus is involved in the regulation of neuropeptide Y (Npy) gene expression in the arcuate nucleus by glucocorticoids. In the hypothalamic organotypic cultures, the incubation with rapamycin significantly inhibited the mTOR signaling which was shown by decreases in the levels of phosphorylated p70S6K1 and S6. Similar to the action of the mTOR inhibitor rapamycin, dexamethasone (DEX), a synthetic glucocorticoid, also inhibited the mTOR signaling in the hypothalamic explants. Analyses of the explants with in situ hybridization demonstrated that the DEX or rapamycin alone significantly increased Npy gene expression in the arcuate nucleus, but that there were no additive effects of DEX and rapamycin on the expression. These data suggest that glucocorticoids upregulate the Npy gene expression in the arcuate nucleus by inhibiting mTOR signaling, at least in part.

本文言語English
ページ(範囲)145-149
ページ数5
ジャーナルPeptides
31
1
DOI
出版ステータスPublished - 01-01-2010
外部発表はい

All Science Journal Classification (ASJC) codes

  • 生化学
  • 生理学
  • 内分泌学
  • 細胞および分子神経科学

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