Lipid Mobilization in Transition Dairy Cows Alters Endothelial Inflammatory Response

Abstract

A hallmark of the transition period in dairy cows is intense lipid mobilization. This mechanism of adaptation is necessary to fulfill the energy deficits experienced by cows in late gestation and early lactation. Lipid mobilization is a dynamic process involving lipolysis and lipogenesis. During the transition period, the rate of lipolysis surpasses that of lipogenesis, inducing the release of non-esterified fatty acids (NEFA) into the blood stream. As a consequence, increased NEFA concentrations disrupt systemic lipid homeostasis not only quantitatively, but also relative to composition. Previous research demonstrated that enhanced lipolysis during the transition period altered the fatty acid composition of different organs and cell populations including blood, liver, adipose tissue, and peripheral blood mononuclear cells. A common change was the increment in the concentrations of saturated fatty acids (palmitic and stearic). Although increments in plasma NEFA are linked to transition cow diseases such as ketosis and displaced abomasum, less is known about the consequences of shifts in fatty acid profiles of endothelial cells and how these changes contribute to dairy cows increased susceptibility to disease. Immune responses are highly dependent on the interactions between immune cells with the vasculature. Indeed, endothelial cells regulate the trafficking of the immune cell migration to and from tissues. We hypothesize that shifts in plasma NEFA content and composition in transition dairy cows modify endothelial cells inflammatory response by enhancing lipid mediator biosynthesis and expression of adhesion molecules.