論文

査読有り
2005年3月

Changes in gene expression of glucose transporters in lactating and nonlactating cows

JOURNAL OF ANIMAL SCIENCE
  • T Komatsu
  • ,
  • F Itoh
  • ,
  • S Kushibiki
  • ,
  • K Hodate

83
3
開始ページ
557
終了ページ
564
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.2527/2005.833557x
出版者・発行元
AMER SOC ANIMAL SCIENCE

Glucose delivery and uptake by the mammary gland are a rate-limiting step in milk synthesis. It is thought that insulin-independent glucose uptake decreases in tissues, except for the mammary gland, and insulin resistance in the whole body increases following the onset of lactation. To study glucose metabolism in peak-, late-, and nonlactating cows, the expression of erythrocyte-type glucose transporter (GLUT1) and the insulin-responsive glucose transporter (GLUT4) in the mammary gland, adipose tissue, and muscle were assessed by Western blotting and real-time PCR. Our results demonstrated that the mammary gland of lactating cows expressed a large amount of GLUT1, whereas the mammary gland of nonlactating cows did not (P < 0.05). On the other hand, adipose tissue of late and nonlactating cows expressed a large amount of GLUT1, whereas the adipose tissue of peak-lactating cows did not (P < 0.05). There were no significant differences in the abundance of GLUT4 mRNA in adipose tissue and muscle, whereas GLUT4 mRNA was not detected in the mammary gland. The plasma insulin concentration was greater (P < 0.05) in nonlactating cows than in peak- and late-lactating cows. The results of the present study indicate that in lactation, GLUT1 expression in the mammary gland and adipose tissue is a major factor for insulin-independent glucose metabolism, and the expression of GLUT4 in muscle and adipose tissue is not an important factor in insulin resistance in lactation; however, the plasma insulin concentration may play a role in insulin-dependent glucose metabolism. Factors other than GLUT4 may be involved in insulin resistance.

リンク情報
DOI
https://doi.org/10.2527/2005.833557x
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000235846500009&DestApp=WOS_CPL
ID情報
  • DOI : 10.2527/2005.833557x
  • ISSN : 0021-8812
  • eISSN : 1525-3163
  • Web of Science ID : WOS:000235846500009

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