Elsevier

Journal of Dairy Science

Volume 95, Issue 10, October 2012, Pages 5709-5719
Journal of Dairy Science

Changes in glucose transporter expression in monocytes of periparturient dairy cows

https://doi.org/10.3168/jds.2012-5327Get rights and content
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Abstract

The transition period of dairy cows is characterized by dramatic changes in metabolism and immune cell function that contributes to increased susceptibility to several economically important diseases. Monocyte and macrophage populations increase in blood and tissues of cows during the transition period and have enhanced inflammatory responses that may contribute to increased severity of disease. Glucose is a major energy source for activated monocytes and glucose uptake is facilitated by glucose transporters (GLUT). The objective of this study was to determine how bovine monocyte GLUT expression changes during lactogenesis and in response to proinflammatory stimulation. Blood samples were collected from 10 dairy cows approximately 5 wk before calving and during the first week of lactation. Monocytes were isolated from total peripheral blood mononuclear cells, and expression of GLUT1, GLUT3, and GLUT4 isoforms was assessed in resting cells and following endotoxin stimulation. In general, the onset of lactation served to decrease overall GLUT expression. Gene and protein expression of GLUT1 was significantly decreased after parturition, and GLUT3 and GLUT4 cell surface expression was also significantly decreased postcalving. Endotoxin stimulation, however, increased gene expression of GLUT3 and GLUT4, and gene expression for all GLUT isoforms was positively correlated to production of tumor necrosis factor-α. This study identified, for the first time, the presence of GLUT isoforms in bovine monocytes. Alterations in monocyte GLUT expression at the onset of lactation warrant further investigation to ascertain how changes in glucose uptake may contribute to periparturient inflammatory dysfunction.

Key words

glucose transporter
monocyte
periparturient period
inflammation

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