Lipid metabolism in lactating ruminants

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Linoleic acid (18:2 n-6) and alpha-linolenic acid (18:3 n-3) are essential nutrients in mammals. These fatty acids and their metabolites are involved in several biological functions, such as immune response, blood coagulation, vascular resistance, cell proliferation and differentiation, enzyme activities, and receptor expression. Ruminants, like other mammals, are not able to synthesize essential fatty acids (EFA); therefore, they must be obtained from feedstuffs. However, there is currently no defined EFA requirements for ruminants. Daily amounts required for lactating cows are hard to establish due to: i) fluctuating proportions of dietary EFA being biohydrogenated in the rumen, reducing their availability for absorption; and ii) varying quantities of n-6 and n-3 fatty acids being secreted in milk fat, which are therefore not available for animal metabolism. With adequate supply of EFA, 18:2 n-6 and 18:3 n-3 are desaturated and elongated to varying metabolites which are important regulators of physiological functions and gene expression. Studies have shown that consumption of greater quantities of EFA may have beneficial effects on hepatic metabolism and lactation performances and in lactating cows. Nevertheless, data are not conclusive enough to define specific intake requirements for an improved efficiency of these systems. The main objective of the proposed research program is to gain further insight into the metabolism of EFA in dairy ruminants. The hypothesis is that EFA supplies in lactating cows modulate hepatic metabolism and the delivery of nutrients to the mammary gland to support milk synthesis. The specific objectives are to: 1) explore the overall adaptations of liver and mammary tissues to EFA deficiency; 2) assess the role of 18:2 n-6 and 18:3 n-3 on animal physiology and lactation performance, when supplied individually or in combination; and 3) study the process of elongation, desaturation and ß-oxidation of EFA. Lactating cows will be fed an EFA-deficient diet. Biopsies will be harvested to determine the impacts on liver and mammary tissue transcriptomes, and blood samples will be collected to determined plasma metabolome. The same model of EFA-deficient cows will be used to further examine the impact of supplemental 18:2 n-6 and 18:3 n-3 on animal physiology. Abomasal infusion of these EFA will allow to study their metabolism (elongation, desaturation) and their effects on molecular and cellular functions, without the uncertainty related to varying rates of ruminal biohydrogenation. By creating a deficiency and controlling intake, biohydrogenation and secretion of EFA, the proposed research program has the potential to more precisely target the metabolic functions requiring 18:2 n-6, 18:3 n-3, or their metabolites. In the long run, this program will allow to define more precise dietary requirements of EFA in lactating ruminants.