Results indicated that the dual marker system of Yb-acetate and Co-EDTA supplied per os reduced the proportion of fatty acids in bovine milk that were products of Delta (9)-desaturase. To verify this effect and identify the responsible marker component, 18 cows (3 cows per treatment) were administered per os a 0.25-L solution of either Co-acetate, Co-EDTA, Co-EDTA + Yb-acetate, EDTA, Yb-acetate, or water twice daily for 5 d. The daily amounts of Co, Yb, and EDTA were, respectively, 3.50, 3.44, and 21.00 g per cow. Milk and blood were sampled and analyzed for content of fatty acids, and blood was sampled and analyzed for Co and cobalamin. Only solutions containing Co had a reducing effect (P < or = 0.01) on fatty acids that were products of Delta(9)-desaturase in milk--cis-9 10:1, cis-9 14:1, cis-9 16:1, cis-9, trans-11 18:2, and cis-9 18:1--with the exception of the solution containing Co-EDTA + Yb-acetate for cis-9 18:1. Of the substrate fatty acids of Delta (9)-desaturase, only 18:0 increased (P < 0.001) in all groups supplied with Co-containing solutions. Thus, Co had a reducing effect (P < or = 0.004) on the Delta (9)-desaturase indices [(product of Delta(9)-desaturase)/(product of Delta(9)-desaturase + substrate of Delta(9)-desaturase)] of milk for cis-9 14:1, cis-9 16:1, cis-9 18:1, and cis-9, trans-11 18:2. There were no differences in Delta(9)-desaturase indices between Co-EDTA and Co-acetate. None of the marker solutions influenced the fatty acid composition of blood plasma, and Co was detected only in the blood samples from cows treated with solutions containing Co. On the basis of these results, we concluded that Co given per os decreased the Delta(9)-desaturase indices of bovine milk.

The objective of this study was to determine whether intravenous infusion of Co affects levels of fatty acid desaturation products in bovine milk. Six cows were assigned to two replicated 3 × 3 Latin squares with 14-day periods. Treatment occurred on days 1 to 5 and depuration occurred on days 6-14. Two treatments were tested, the first consisting of per os supplementation of 3.5 g Co daily in the form of Co acetate and the second consisting of intravenous injection of 175 mg Co daily in the form of Co acetate diluted in saline solution. The third treatment was a control. Both Co treatments decreased cis-9 18:1 levels from approximately 18 to 14 g/100 g fatty acids, and increased 18:0 levels from 11 to 17 g/100 g fatty acids in milk fat (p < 0.001). The proportions of cis-9 10:1, cis-9 12:1, cis-9 14:1, cis-9 16:1 and cis-9 17:1 decreased (p < 0.001), whereas 17:0 and trans-11 18:1 increased (p < 0.001). In blood plasma, levels of cis (6,9,12) 18:3 (p < 0.001) and cis (8,11,14,17) 20:4 (p = 0.008) decreased after both the Co treatments. It is concluded that intravenous supply of Co reduces levels of fatty acid desaturation products in both bovine milk and blood.

No abstract

The main objective of this study was to investigate the effect of excess cobalt (Co) on gene expression of stearoyl-CoA desaturase (SCD), fatty acid synthase (FASN), diacylglycerol acyltransferase 1 (DGAT1) and diacylglycerol acyltransferase 2 (DGAT2) of lactating dairy cows in relation to milk fatty acid profile. Seven multiparous cows of the Norwegian Red cattle breed (NRF) had their basal diet supplemented with 1.4 g Co as a 24 g/l solution of Co-acetate per os twice daily for 7 days followed by a 9-day depuration period. Udder biopsies were performed prior to the treatment period, after 1 week of treatment and immediately after the depuration period. Excess Co reduced the proportion of all cis-9 monounsaturated fatty acids and increased the proportion of 18:0 in milk. However, gene expression levels of SCD, DGAT1, DGAT2 and FASN were not significantly altered. Our results indicate that the effect of Co on milk fatty acid profile is mediated at the post-transcriptional level by reduced activity of SCD in the mammary gland. Potential mechanisms explaining how Co might reduce stearoyl-CoA desaturation are discussed.

Summary Twelve sows received a supplement of 50 ml cod liver oil, without vitamin A and D, daily from day 107 of gestation until weaning. Eight sows served as control. A milk sample was obtained from each sow at parturition and on day 14 of lactation. The piglets were weighed at birth, on days 7, 14 and on the day of weaning. Eicosapentaenoic acid (20:5, n‐3) (EPA), docosahexaenoic acid (22:6, n‐3) (DHA) and docosapentaenoic acid; (22:5, n‐3) (DPA) were found in milk fat from all sows. At parturition the contents of EPA, DPA and DHA were significantly higher in the group given cod liver oil supplement. After 2 weeks of lactation only EPA and DHA were elevated compared with the non‐supplemented group. No effect on weight gain or on the overall morbidity of the piglets was found. The animal health in this farm was very good, and the growth rate faster than the average for Norwegian pigs.