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著作: Sasaki Tsutomu/Kim Hye-Jin/Kobayashi Masaki/Kitamura Yukari-Ido/Yokota-Hashimoto Hiromi/[志内 哲也]/Minokoshi Yasuhiko/Kitamura Tadahiro/Induction of hypothalamic Sirt1 leads to cessation of feeding via agouti-related peptide./[Endocrinology]

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EID
221420
EOID
654583
Map
0
LastModified
2012年8月29日(水) 12:46:28
Operator
大家 隆弘
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TRUE
Censor
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Owner
志内 哲也
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種別 必須 学術論文(審査論文)
言語 必須 英語
招待 推奨
審査 推奨
カテゴリ 推奨
共著種別 推奨
学究種別 推奨
組織 推奨
著者 必須
  1. (英) Sasaki Tsutomu
    役割 任意
    貢献度 任意
    学籍番号 推奨
  2. (英) Kim Hye-Jin
    役割 任意
    貢献度 任意
    学籍番号 推奨
  3. (英) Kobayashi Masaki
    役割 任意
    貢献度 任意
    学籍番号 推奨
  4. (英) Kitamura Yukari-Ido
    役割 任意
    貢献度 任意
    学籍番号 推奨
  5. (英) Yokota-Hashimoto Hiromi
    役割 任意
    貢献度 任意
    学籍番号 推奨
  6. 志内 哲也([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.生理系.統合生理学])
    役割 任意
    貢献度 任意
    学籍番号 推奨
  7. (英) Minokoshi Yasuhiko
    役割 任意
    貢献度 任意
    学籍番号 推奨
  8. (英) Kitamura Tadahiro
    役割 任意
    貢献度 任意
    学籍番号 推奨
題名 必須

(英) Induction of hypothalamic Sirt1 leads to cessation of feeding via agouti-related peptide.

副題 任意
要約 任意

(英) Silent information regulator (SIR)2 is an nicotinamide adenine dinucleotide dependent deacetylase implicated in the regulation of life span in species as diverse as yeast, worms, and flies. Mammalian Sirt1 is the most closely related homolog of the SIR2 gene. Pharmacological activators of Sirt1 have been reported to increase the life span and improve the health of mice fed a high-fat diet and to reverse diabetes in rodents. Sirt1 links the energy availability status with cellular metabolism in peripheral organs including liver, pancreas, muscle, and white adipose tissue. Insulin and leptin signaling regulate food intake by controlling the expression of orexigenic and anorexigenic neuropeptides in the arcuate nucleus of the hypothalamus via Forkhead box O (Foxo)-1 and signal transducer and activator of transcription-3. Sirt1 has been reported to improve insulin sensitivity in vitro, but the role of hypothalamic Sirt1 in regulating feeding has not been addressed. We found that hypothalamic Sirt1 protein levels increase on feeding, and this induction is abrogated in diet-induced obese mice and db/db mice. We also demonstrate for the first time that Sirt1 protein turnover is regulated by the proteasome and ubiquitination in a hypothalamic cell line and in vivo by feeding, and this regulation is not seen in a pituitary cell line AtT20. Forced expression of wild-type Sirt1 in the mediobasal hypothalamus by adenovirus microinjection suppressed Foxo1-induced hyperphagia, a model for central insulin resistance. Moreover, Sirt1 suppressed Foxo1-dependent expression of the orexigenic neuropeptide Agouti-related peptide in vitro. We propose that on feeding, Sirt1 protein is stabilized in the hypothalamus, leading to decreased Foxo1-dependent expression of orexigenic neuropeptide Agouti-related peptide and cessation of feeding.

キーワード 推奨
  1. (英) Animals
  2. (英) Blotting, Western
  3. (英) Cell Line
  4. (英) Feeding Behavior
  5. (英) Forkhead Transcription Factors
  6. (英) Humans
  7. (英) Hyperphagia
  8. (英) Hypothalamus
  9. (英) Immunohistochemistry
  10. (英) Immunoprecipitation
  11. (英) Male
  12. (英) Mice
  13. (英) Mice, Inbred C57BL
  14. (英) Proteasome Endopeptidase Complex
  15. (英) Reverse Transcriptase Polymerase Chain Reaction
  16. (英) Sirtuin 1
  17. (英) Weight Gain
発行所 推奨
誌名 必須 Endocrinology([The Endocrine Society])
(pISSN: 0013-7227, eISSN: 1945-7170)
ISSN 任意 1945-7170
ISSN: 0013-7227 (pISSN: 0013-7227, eISSN: 1945-7170)
Title: Endocrinology
Title(ISO): Endocrinology
Publisher: Endocrine Society
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
必須 151
必須 6
必須 2556 2566
都市 任意
年月日 必須 2010年 4月 7日
URL 任意
DOI 任意 10.1210/en.2009-1319    (→Scopusで検索)
PMID 任意 20375183    (→Scopusで検索)
NAID 任意
WOS 任意
Scopus 任意
評価値 任意
被引用数 任意
指導教員 推奨
備考 任意
  1. (英) Affiliation: Metabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi, Maebashi-shi, Gunma 371-8512, Japan.

  2. (英) PublicationType: Journal Article

  3. (英) PublicationType: Research Support, Non-U.S. Gov't