Changes in the gene expression of adiponectin and glucose transporter 12 (GLUT12) in lactating and non-lactating cows

Glucose delivery and uptake by the mammary gland is a rate-limiting step in milk synthesis. Insulin resistance is believed to increase throughout the body following the onset of lactation. To study glucose metabolism in peak-, fate-, and non-lactating cows we analyzed the expression of an adipokine,...

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Veröffentlicht in:Animal science journal 2007-02, Vol.78 (1), p.98-102
Hauptverfasser: Komatsu, T.(National Inst. of Livestock and Grassland Science, Tsukuba, Ibaraki (Japan)), Itoh, F, Sakumoto, R, Hodate, K, Obara, Y, Kushibiki, S
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Sprache:eng
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Zusammenfassung:Glucose delivery and uptake by the mammary gland is a rate-limiting step in milk synthesis. Insulin resistance is believed to increase throughout the body following the onset of lactation. To study glucose metabolism in peak-, fate-, and non-lactating cows we analyzed the expression of an adipokine, namely, adiponectin, decreased insulin resistance, leptin, and a novel insulin-responsive glucose transporter (GLUT12) in the adipose tissue and mammary gland by using real-time polymerase chain reaction. Our results demonstrated that the mRNA level of adiponectin in the adipose tissue was greater in non-lactating cows than in peak-lactating cows. In the adipose tissue, there were no significant differences in the abundance of GLUT12 mRNA between the peak-, late-, and non-lactating cows. In contrast, in the mammary gland, the mRNA level of GLUT12 was greater in non-lactating cows than in peak- and late-lactating cows. In the adipose tissue, the mRNA level of leptin and peroxisome proliferator-activated receptor gamma 2 (PPARgamma2) was greater in non-lactating cows than in peak-lactating cows. The results of the present study suggest that in lactating cows adiponectin plays an important role in insulin resistance in the adipose tissue; in the mammary gland, GLUT12 expression is believed to be an important factor for insulin-dependent glucose metabolism.
ISSN:1344-3941
1740-0929
DOI:10.1111/j.1740-0929.2006.00411.x