論文

査読有り
2014年8月

Decreased Gene Expressions of Insulin Signal Molecules in Canine Hyperadrenocorticism

JOURNAL OF VETERINARY MEDICAL SCIENCE
  • Satoshi Nozawa
  • ,
  • Hitomi Oda
  • ,
  • Ran Akiyama
  • ,
  • Kaori Ueda
  • ,
  • Kaori Saeki
  • ,
  • Saori Shono
  • ,
  • Natsuki Maruyama
  • ,
  • Atsuki Murata
  • ,
  • Hiroyuki Tazaki
  • ,
  • Akihiro Mori
  • ,
  • Yutaka Momota
  • ,
  • Daigo Azakami
  • ,
  • Toshinori Sako
  • ,
  • Katsumi Ishioka

76
8
開始ページ
1177
終了ページ
1182
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1292/jvms.14-0033
出版者・発行元
JAPAN SOC VET SCI

Hyperadrenocorticism (HAC) is a common endocrine disorder in dogs, in which excess glucocorticoid causes insulin resistance. Disturbance of insulin action may be caused by multiple factors, including transcriptional modulation of insulin signal molecules which lie downstream of insulin binding to insulin receptors. In this study, gene expressions of insulin signal molecules were examined using neutrophils of the HAC dogs (the untreated dogs and the dogs which had been treated with trilostane). Insulin receptor substrate (IRS)-1, IRS-2, phosphatidylinositol 3-kinase (P13-K), protein kinase B/Akt kinase (Akt)-2 and protein kinase C (PKC)-lambda were analyzed in the HAC dogs and compared with those from normal dogs. The IRS-1 gene expressions decreased by 37% and 35% of the control dogs in the untreated and treated groups, respectively. The IRS-2 gene expressions decreased by 61% and 72%, the P13-K gene expressions decreased by 47% and 55%, and the Akt-2 gene expressions decreased by 45% and 56% of the control dogs, similarly. Collectively, gene expressions of insulin signal molecules are suppressed in the HAC dogs, which may partially contribute to the induction of insulin resistance.


リンク情報
DOI
https://doi.org/10.1292/jvms.14-0033
J-GLOBAL
https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201402271000441622
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/24829079
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000341904000019&DestApp=WOS_CPL