Effect of dietary supplementation of sodium acetate and calcium butyrate on milk fat synthesis in lactating dairy cows.

Acetate is a major source of energy and substrate for milk fat synthesis in the dairy cow. We recently reported a linear increase in milk fat yield and greater than a 30% net apparent transfer of acetate to milk fat with ruminal infusion of neutralized acetate. Additionally, ruminal acetate infusion linearly increases plasma ß-hydroxybutyrate. The objective of the current study was to investigate the ability of acetate and butyrate fed in a diet to increase milk fat synthesis. Twelve multiparous lactating Holstein cows were randomly assigned to treatments in a 3 × 3 Latin square design with 14-d periods that included a 7-d washout followed by 7 d of treatment. Cows were fed ad libitum a basal diet with a low risk for biohydrogenation-induced milk fat depression, and treatments were mixed into the basal diet. Treatments were 3.2% NaHCO3 (control), 2.9% sodium acetate, and 2.5% calcium butyrate (carbon equivalent to acetate treatment) as a percent of diet dry matter. Feeding sodium acetate increased dry matter intake by 2.7 kg, had no effect on milk yield, and increased milk fat yield by 90 g/d and concentration by 0.2 percentage units, compared with control. Calcium butyrate decreased dry matter intake by 2.6 kg/d, milk yield by 1.65 kg/d, and milk fat yield by 60 g/d, compared with control. Sodium acetate increased concentration and yield of 16 carbon mixed source fatty acids (FA) and myristic acid, while decreasing the concentration of preformed FA, compared with control. Calcium butyrate had no effect on concentration of milk FA by source, but increased concentration of trans-10 C18:1 in milk by 18%, indicating a shift in rumen biohydrogenation pathways. Our data demonstrate that milk fat yield and concentration can be increased by feeding sodium acetate at 2.9% of diet dry matter, but not by feeding calcium butyrate at an equivalent carbon mass.

Peroxisome proliferator-activated receptor gamma (PPARγ) agonist fails to overcome trans-10, cis-12 conjugated linoleic acid (CLA) inhibition of milk fat in dairy sheep.

The trans-10, cis-12 conjugated linoleic acid (CLA) causes milk fat depression by downregulating expression of genes and transcription factors involved in lipogenesis and it has been proposed that peroxisome proliferator-activated receptor gamma (PPARγ) can be inhibited by trans-10, cis-12 CLA. The PPARγ is a nuclear receptor activated by natural or synthetic ligands and promotes expression of lipogenic genes and its effect on mammary lipogenesis and the interaction with trans-10, cis-12 CLA in lactating ewes was evaluated using thiazolidinedione (TZD), a chemical PPARγ agonist. A total of 24 lactating ewes were randomly assigned to one of the following treatments for 7 days: (1) Control (5 ml/day of saline solution); (2) TZD (4 mg/kg of BW/day in 5 ml of saline solution); (3) CLA (27 g/day with 29.9% of trans-10, cis-12); (4) TZD+CLA. Compared with Control, milk fat content was not changed by TZD, but was decreased 22.3% and 20.5% by CLA and TZD+CLA treatments. In the mammary gland, TZD increased PPARγ gene expression by 174.8% and 207.8% compared with Control and TZD+CLA treatments, respectively. Conjugated linoleic acid reduced sterol regulatory element-binding transcription protein 1 (SREBP1) gene expression 89.2% and 75.3% compared with Control and TZD+CLA, respectively, demonstrating that TZD fails to overcome CLA inhibition of SREBP1 signaling. In adipose tissue, the expression of SREBP1 and stearoyl CoA desaturase 1 (SCD1) genes were increased by the TZD+CLA treatment, compared with the other treatments. Conjugated linoleic acid decreased milk fat concentration and expression of lipogenic genes, while TZD had no effect on milk fat concentration, expression of lipogenic enzymes or regulators in the mammary gland and failed to overcome the inhibition of these by CLA. Therefore, CLA inhibition of milk fat synthesis was independent of the PPARγ pathway in lactating dairy ewes.

Acetate Dose-Dependently Stimulates Milk Fat Synthesis in Lactating Dairy Cows.

Background: Acetate is a short-chain fatty acid (FA) that is especially important to cows because it is the major substrate for de novo FA synthesis. However, the effect of acetate supply on mammary lipid synthesis is not clear.Objective: The objective of this experiment was to determine the effect of increasing acetate supply on milk fat synthesis in lactating dairy cows.Methods: Six multiparous lactating Holstein cows were randomly assigned to treatments in a replicated design to investigate the effect of acetate supply on milk fat synthesis. Treatments were 0 (control), 5, 10, and 15 mol acetate/d continuously infused into the rumen for 4 d. Rumen short-chain FAs, plasma hormones and metabolites, milk fat concentration, and milk FA profile were analyzed on day 4 of each treatment. Polynomial contrasts were used to test the linear and quadratic effects of increasing acetate supply.Results: Acetate increased milk fat yield quadratically (P < 0.01) by 7%, 16%, and 14% and increased milk fat concentration linearly (P < 0.001) by 6%, 9%, and 11% for 5, 10, and 15 mol acetate/d, respectively, compared with the control treatment. Increased milk fat yield predominantly was due to a linear increase in 16-carbon FAs (P < 0.001) and a quadratic increase in de novo synthesized FAs (<16-carbon FAs; P < 0.01), indicating that there was stimulation of de novo synthesis pathways. Apparent transfer of acetate to milk fat was 33.4%, 36.2%, and 20.6% for 5, 10, and 15 mol/d, respectively. Acetate infusion linearly increased the relative concentration of rumen acetate (P < 0.001) before feeding, but not after feeding. Acetate linearly increased plasma ß-hydroxybutyric acid by 29%, 50%, and 78%, respectively, after feeding compared with the control treatment (P < 0.01).Conclusions: Increasing acetate supply to lactating cows increases milk fat synthesis, suggesting that nutritional strategies that increase ruminal acetate absorption would be expected to increase milk fat by increasing de novo FA synthesis.