2014年8月
Decreased Gene Expressions of Insulin Signal Molecules in Canine Hyperadrenocorticism
JOURNAL OF VETERINARY MEDICAL SCIENCE
- 巻
- 76
- 号
- 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
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- 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
- URL
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84906853232&origin=inward
- ID情報
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- DOI : 10.1292/jvms.14-0033
- ISSN : 0916-7250
- eISSN : 1347-7439
- J-Global ID : 201402271000441622
- PubMed ID : 24829079
- SCOPUS ID : 84906853232
- Web of Science ID : WOS:000341904000019