Supplementing fish oil to dairy cattle: Effects on metabolism and immune responses

Neonatal dairy calves experience high incidences of morbidity and mortality. The pathogenesis of septicemia is a major cause of the high mortality. In addition, peripartum, multiparous cows are more susceptible to the deleterious local and systemic effects of coliform mastitis. The acute phase responses (APR) of both calves and peripartum cows are intact, and may be too aggressive, which is an underlying cause for the severe pathogenesis. In addition, multiparous cows are susceptible to hepatic steatosis immediately postpartum. Supplementing the omega-3 FA in fish oil (FO), eicosapentaenoic (EPA) and docosahexaenoic (DHA), decreased the pathogenesis of the APR and decreased 1ipogenesis and increased lipid oxidation in rodents and humans. Therefore, supplementing FO to neonatal calves and peripartum cows may benefit their health if n-3 FA limits the acute phase response and partition lipids away from synthesis and towards oxidation.;Supplementing peripartum, multiparous cows with FO compared with a saturated lipid supplement did not influence the anti-microbial activity of whole blood, the interferon-gamma or tumor necrosis factor-alpha production of PBMC, or the pathophysiological response to an intramammary endotoxin challenge. Supplemental lipid, regardless of the FA composition, improved the metabolic status, increased plasma glucose, and decreased non-esterified FA and beta-hydroxybutyrate concentrations of peripartum cows. Despite significantly altered FA composition of hepatocytes in FO cows, there was no effect of lipid supplementation or the source of the lipid supplement on the accumulation of hepatic TG. Supplemental FO modulated immune responses of neonatal calves, but had no effect on either the metabolism or immune responses of peripartum cows.;Supplementing neonatal calves with FO increased the proportions of EPA and DHA in both the plasma and peripheral blood mononuclear cell (PBMC) pools as well as moderately attenuated the pathogenesis of the APR. The effects were linear with increasing FO in the milk replacer. Supplementing milk replacer with FO had quadratic effects on both the oxidative burst capacity of neutrophils and the secondary humoral response to ovalbumin. The intermediate dose of FO increased the oxidative burst, but attenuated the secondary humoral response. There was no effect of supplemental FO on any production or health variable.