CONTROLLED MILK FAT DEPRESSION AS A MANAGEMENT TOOL TO IMPROVE ENERGY BALANCE IN LACTATING DAIRY CATTLE

Abstract

Research conducted for this dissertation had three goals; 1) determine if CLA can induce milk fat depression immediately postpartum, 2) determine if CLA can alter energy availability, 3) determine the mechanism behind the mammary gland's decreased sensitivity to CLA immediately postpartum. The first study provides strong evidence indicating CLA can decrease milk fat synthesis immediately postpartum, but the dose required is approximately 3x greater than in established lactation. This trial also provided evidence that CLA can alter energy status, as CLA decreased days to EBAL nadir by nearly 5 days. This is relevant as recovery of EBAL from its lowest point provides an important signal for initiating ovarian activity and days to nadir is highly correlated with days to first ovulation. Study two was designed to determine if CLA induced milk fat depression could improve energy status during heat stress. Rumen-inert CLA reduced milk fat synthesis, and was able to improve energy availability, but did not increase milk yield or yield of other milk components. Although production was unchanged in this study, the study did provide further evidence that rumen-inert CLA can alter energy availability. Study three utilized intravenous infusion of CLA in cows in mid and early lactation to determine the mechanism for the mammary gland's decreased sensitivity in early lactation. It is postulated that increased fatty acid oxidation and subsequent enhanced levels of circulating NEFA present during the transition period competitively prevent adequate CLA uptake by the mammary gland. In the current study, trans-10, cis-12 CLA concentration in milk was not different between early and established lactation, while milk fat yield was drastically reduced on d 4 and 5 of trans-10, cis-12 CLA infusion in mid lactation cows, but unaltered in early lactation. Further, NEFA levels were nearly 3 fold higher in early lactation than in mid lactation, providing further evidence that increased circulating NEFAs in early lactation are unlikely to be the source of the mammary gland's decreased sensitivity during this time. Do to the variation in gene expression observed in this trial, we were unable to make any definitive conclusions as to the sensitivity of the expression of genes involved in milk lipid synthesis to CLA in early vs. mid lactation.