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Sixteen Holstein cows in mid-lactation were used to determine whether alterations of mammary fatty acid metabolism are responsible for the milk fat depression associated with consumption of fish oil. Cows were given a total mixed ration with no added fish oil (control), unprotected fish oil (3.7% of dry matter), or glutaraldehyde-protected microcapsules of fish oil (1.5% or 3.0% of dry matter) for 4 weeks. Milk samples were taken once a week and a mammary biopsy was taken from a rear quarter at the end of the treatment period. Milk fat content was lower in cows given unprotected fish oil (26.0 g/kg), 1.5% protected fish oil (24.6 g/kg) and 3% protected fish oil (20.4 g/kg) than in cows fed the control diet (36.0 g/kg). This was mainly due to a decrease in the synthesis of short-chain fatty acids. Consumption of protected fish oil decreased the abundance of lipogenic enzymes mRNA in the mammary gland. Acetyl-CoA carboxylase, fatty acid synthase, and stearoyl-CoA desaturase mRNAs for cows given 3% protected fish oil averaged only 30%, 25% and 25% of control values, respectively. Dietary addition of unprotected fish oil slightly decreased mRNA abundance of these enzymes but markedly reduced the amount of lipoprotein lipase mRNA. Milk fat content was significantly correlated with gene expression of acetyl-CoA carboxylase, fatty acid synthase, and stearoyl-CoA desaturase but not lipoprotein lipase. These results suggest that fish oil reduces milk fat percentage by inhibiting gene expression of mammary lipogenic enzymes.

Our objective was to determine the influence of bovine growth hormone (bGH) and bovine growth hormone-releasing factor (bGRF) administration on the mRNA abundance of lipoprotein lipase (LpL) and stearoyl-CoA desaturase (SCD). Primiparous Holstein cows received bGH, bGRF, or no treatment from 118 to 181+/-1 d postpartum. We hypothesized that bGH and bGRF treatment would increase the mRNA abundance of both SCD and LpL in the mammary gland with a corresponding reduction in adipose tissue. Milk yield significantly increased but milk fat percentage did not change as a result of bGH or bGRF treatment. Short-, medium-, and long-chain fatty acid concentrations in milk were not affected by either bGH or bGRF treatments, with the exception of a modest, but significant, increase in C16:1 and C18:1 following bGH treatment. Analysis was conducted on the genes encoding LpL (E.C. 3.3.1.34), a key enzyme involved in the uptake of fatty acids into tissues, and SCD (E.C. 1.14.99.5), which is the enzyme responsible for introducing delta9 double bonds in fatty acids of 16 and 18 carbons in length. In adipose tissue, treatment with bGH and bGRF reduced the mRNA abundance of LpL to 14.6 and 25.7% respectively, of that observed for control animals. Similarly, these treatments reduced the SCD mRNA abundance to undetectable levels in adipose tissue. In mammary gland, bGH and bGRF had no significant impact on LpL mRNA abundance. Bovine GH did not significantly affect SCD mRNA abundance in the mammary gland, and bGRF reduced SCD mRNA abundance. From this study to examine the role of bGH and bGRF on the expression of the genes encoding these key lipogenic enzymes in cattle, we conclude that the increased substrate required for enhanced milk fatty acid yield may have been provided through redirection of nutrients to the mammary gland away from adipose tissue and through overall increased metabolism in the mammary gland.

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