The effect of dietary P content on P partitioning and excretion during early lactation was evaluated in 13 cows fed diets containing 0.34 (no supplementary P), 0.51, or 0.67% P. All cows were fed a common pre-partum total mixed ration (TMR) (0.28% P), followed by common TMR (0.51% P) for 7 d post-partum. On day 7, cows were randomly assigned to one of the three dietary P treatments. All treatment diets contained 16.6% CP, 15.2% ADF, 26.3% NDF, and 0.74% Ca. Total collections of milk, urine, and feces were conducted during weeks 3, 5, 7, 9, and 11 of lactation. Average body weight (591 kg), milk yield (47.9 kg/d), and DMI (25.2 kg/d) throughout the 10-wk trial were not affected by dietary P content. With increasing dietary P, however, linear increases in P intake (84.7, 135.2, and 161.5 g/d), fecal P (42.3, 87.5, and 108.6 g/d), urinary P (0.32, 1.28, and 3.90 g/d), and total P excretion (42.6, 88.8, and 112.5 g/d) were observed. Apparent P digestibility (49.0, 34.4, and 32.8% of P intake) decreased quadratically with increasing dietary P. Phosphorus balance was highly variable, but cows fed the 0.34% P diet were in negative P balance longer than were cows fed diets containing 0.51 or 0.67% P. With increasing dietary P, serum concentrations of inorganic P increased linearly, but serum Ca and Mg concentrations decreased. Increasing dietary P increased fecal and urinary P excretion in early lactation cows. Increased duration of negative P balance and changes in blood mineral concentrations suggest that cows fed low P diets mobilized more P from body reserves than cows on medium- and high-P diets.

To determine effects of an elevated supply of cis9,trans11-18:2 (9/11CLA) or trans10,cis12-18:2 (10/12CLA) on de novo synthesis and desaturation of long-chain fatty acids, four Holstein cows fed high-oleic sunflower (OLE) or high-linoleic safflower oil (LIN) at 2.5% of DM were infused (0.625 g/h) with 9/11CLA or 10/12CLA for 48 h via the abomasum. Treatments were assigned in a 2 x 2 factorial design. The assigned diets were fed for 11 d before each 48-h infusion period. Milk samples were obtained at 12 and 0 h before infusion and at 12-h intervals from 0 to 96 h. Concentrations of trans11-18:1 and 18:2n-6 in arterial plasma phospholipid, triglyceride, and FFA fractions were greater due to feeding LIN compared with OLE. Infused 9/11CLA and 10/12CLA were incorporated into plasma triglycerides and FFA primarily. Exogenous 10/12CLA also was found in plasma phospholipids. Milk yield and DMI were not affected by treatments. Percentages and yields of protein, lactose, and SNF in milk also were not affected by treatments. Milk fat percentage and yield, however, decreased 25% from 0 to 96 h in response to infusion of 10/12CLA compared with 9/11CLA. Yields of trans11-18:1, 9/11CLA and 18:2n-6 in milk fat before infusion were higher when LIN was fed compared with OLE. Infusion of 9/11CLA, regardless of diet, increased 9/11CLA in milk fat by 44%. Although 10/12CLA was not detectable in milk fat before infusion, it averaged 6 mg/g of total fatty acids and 2 g/d after 48 h. At 48 h, recovery in milk of infused 9/11CLA was 16% compared with 8% for 10/12CLA. Yields of saturated 6:0 to 16:0, cis9-18:1, 9/11CLA, and 20:4n-6 were reduced by 10/12CLA infusion. Due to a 40% increase in the concentration of 18:0 by 48 h of 10/12CLA infusion, however, yield of 18:0 was not affected. Ratios of cis9-18:1/18:0, 9/11CLA/trans11-18:1, and 20:4n-6/18:2n-6 in milk fat decreased in response to infusion of 10/12CLA, regardless of diet. At peak concentration of 10/12CLA, reductions in cis9-18:1 and saturated 4:0-16:0 yields accounted for 36% and 53% of the decrease in total fatty acid yield. Results indicated 10/12CLA alters lipid metabolism in the bovine mammary gland by simultaneously reducing de novo synthesis and desaturation. Furthermore, milk triglyceride synthesis may have a stringent requirement for endogenously synthesized oleic acid.

Conjugated linoleic acid (CLA) is a potent anticarcinogen secreted in milk of ruminants, but it inhibits de novo fatty acid synthesis and desaturation in mammary cell cultures. The potential for increasing CLA content of milk fat and the effects of elevated CLA availability on milk fat secretion were investigated. Four Holstein cows were used in a single crossover design with repeated measures to determine milk fatty acid concentration in response to a 24-h infusion of 200 g linoleic acid (LA) or a mixture of 100 g LA plus 100 g CLA (LCLA). Milk and blood samples were obtained 12 h before infusion and at 12-h intervals from 0 to 72 h. Compared with LA infusion, total CLA concentration in blood plasma at 24 h in response to LCLA was elevated fivefold, whereas CLA content of plasma triglycerides was increased 10-fold. Milk fat yield from 24 to 72 h was approximately 34% lower in response to LCLA compared with LA, due primarily to reduced yield of fatty acids with six to 16 carbons. Amount of CLA in milk increased from 0.5 g/100 g total fatty acids at 0 h to 3.3 g/100 g at 36 h in response to LCLA. Concentration of stearic acid in milk fat at 36 h in response to LCLA was nearly double the stearic acid concentration in response to LA. Oleic and arachidonic acid concentrations in milk declined as stearic acid increased in response to LCLA. Results indicated CLA content of milk fat reflects the amount available for absorption from the small intestine, and CLA appeared to be a potent inhibitor of de novo fatty acid synthesis and desaturation in the mammary gland.

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