Gene expression of hepatic gluconeogenic and fatty acid metabolism in early-lactation dairy cows as affected by dietary starch and monensin supplementation.

Our previously published companion papers demonstrated improved production performance and energetic metabolism in cows fed diets with increased propiogenic potential in early lactation. Study objectives were to further explore effects of dietary starch content and monensin on hepatic gene expression of key enzymes related to gluconeogenesis and fatty acid metabolism in early lactation. From d 1 to 21 postpartum, primiparous (n = 16) and multiparous (n = 33) Holstein cows were fed a high (HS; 26.2% starch, 34.3% neutral detergent fiber, 22.7% acid detergent fiber, 15.5% crude protein) or low (LS; 21.5% starch, 36.9% neutral detergent fiber, 25.2% acid detergent fiber, 15.4% crude protein) starch diet with a daily topdress containing either 0 (Con) or 450 mg/d monensin (Mon). Cows were randomly assigned to treatment. Liver biopsies were obtained from cows on d 7 postpartum for DNA and RNA quantification and mRNA expression analysis. In primiparous cows, Mon supplementation decreased CPT1A expression relative to controls, whereas in multiparous cows Mon increased its expression. Cows fed HS and Mon tended to have decreased HMGCS2 expression relative to cows fed HS and Con. In multiparous cows, Mon supplementation tended to increase PC and PCK1 expression relative to controls. Correlation analysis was performed for all gene expression variables. Overall, relationships were similar in directionality and magnitude between cows fed HS and LS and Con and Mon. However, for cows fed Con there was a positive relationship between HMGCS2 and PC and HMGCS2 and PCK1, whereas for cows fed Mon there was no relationship. There was a similar lack of relationship between HMGCS2 and PC for cows fed HS. Overall, results support changes in performance and energetic metabolism reported in our companion papers, indicating that cows fed diets of different starch content in early lactation with Mon supplementation throughout the transition period had alterations in hepatic gene expression consistent with increased hepatic propionate supply.

Effect of monensin on milk production efficiency and milk composition in lactating dairy cows fed modern diets.

Since the US Food and Drug Administration's approval of monensin in 2004, significant nutritional advances have been made to increase feed efficiency and milk fat production. Recent evidence suggests monensin's adverse effect on milk fat percentage may be absent when diets are formulated to address known diet-induced milk fat depression risk factors. Thus, study objectives were to evaluate effects of monensin level on dry matter intake (DMI), milk production and composition, and efficiency of high-producing cows fed diets formulated to optimize milk fat. Ninety-six lactating Holstein cows (36 primiparous, 60 multiparous; 106 ± 17 d in milk [DIM]) were balanced by parity, DIM, and milk production and were randomly assigned to 1 of 12 pens with 8 cows per pen. All cows received 11 g/t monensin for 5 wk after which pens received 1 of 4 dietary treatments (n = 3) formulated to provide 0 (CON), 11 (R11), 14.5 (R14.5), or 18 (R18) g/t monensin for 9 wk. The basal diet was 54% forage, 27% NDF, 29% starch, and 2.3% rumen unsaturated fatty acid load. Pen was the experimental unit and data were analyzed using the Fit Model Procedure of JMP. Effects of treatment, time, and treatment × time interaction were included as fixed effects and pen as a random effect. Least squares means were determined and linear and quadratic contrasts were tested. Dry matter intake tended to decrease linearly with increasing monensin dose. Milk yield, fat percentage, and protein percentage and yield were unaffected by treatment while fat yield was quadratically increased. Milk de novo and mixed fatty acid (FA) yields (g/d) increased quadratically with monensin whereas preformed FA linearly decreased during the experimental period. Energy-corrected milk (ECM) was quadratically increased by monensin. Milk urea nitrogen concentrations increased linearly with increasing monensin dose. Monensin linearly increased feed efficiency (ECM/DMI, 3.5% fat-corrected milk/DMI, and solids-corrected milk/DMI). Body weight gain did not differ between treatments. Estimated dietary energy tended to increase linearly with increasing monensin level. These data suggest monensin improves component-corrected milk production efficiency, estimated dietary energy, and does not negatively affect milk fat percentage or FA profile.

Effect of diet fermentability and unsaturated fatty acid concentration on recovery from diet-induced milk fat depression.

Diet-induced milk fat depression is caused by highly fermentable and high-unsaturated fatty acid (FA) diets, and results in reduced milk fat concentration and yield, reduced de novo FA, and increased trans isomers of the alternate biohydrogenation pathways. The hypothesis of the current experiment was that a diet higher in fermentability and lower in unsaturated FA (UFA) would accelerate recovery compared with a high-UFA and lower-fermentability diet. Eight ruminally cannulated and 9 noncannulated multiparous Holstein cows were randomly assigned to treatment sequences in a replicated Latin square design. During each period milk fat depression was induced for 10 d by feeding a low-fiber, high-UFA diet [25.9% neutral detergent fiber (NDF) and 3.3% C18:2]. Following the induction phase, cows were switched to recovery treatments for 18 d designed to correct dietary fermentability, UFA, or both fermentability and UFA concentration. Treatments during recovery were (1) correction of fiber and UFA diet [control; 31.8% NDF and 1.65% C18:2], (2) a diet predominantly correcting fiber, but not UFA [high oil (HO); 31.3% NDF and 2.99% C18:2], and (3) a diet predominantly correcting UFA, but not fiber concentration [low fiber (LF); 28.4% NDF and 1.71% C18:2]. Milk and milk component yield, milk FA profile, ruminal pH, and 11 rumen microbial taxa were measured every third day during recovery. Milk yield decreased progressively in HO and control, whereas it was maintained in the LF diet. Milk fat concentration increased progressively during recovery in all treatments, but was on average 9% lower in LF than control from d 12 to 18. Milk fat yield increased progressively in all treatments and was not different between control and LF at any time point, but was lower in HO than control on d 15. Milk trans-10 C18:1 and trans-10,cis-12 conjugated linoleic acid decreased progressively in all treatments, but was higher in HO than control from d 3 to 18 [136 ± 50 and 188 ± 57% (mean ± SD)], whereas LF caused a smaller increase in these FA compared with control (67 ± 25 and 90 ± 22%). Additionally, milk trans-11 C18:1 and cis-9,trans-11 conjugated linoleic acid was decreased in control and LF and increased in HO during recovery. Selected microbial species observed changed during recovery, but major treatment differences were only observed for Streptococcus bovis. The LF diet that was similar in UFA but 3.4% units lower in NDF compared with to the control had a similar decrease in alternate trans biohydrogenation intermediates in milk. The HO diet that was similar in NDF but 2.0% units higher in UFA compared with the control had higher alternate trans biohydrogenation intermediates in milk compared with control. However, recovery of milk fat yield was similar between treatments at most time points.

Effect of monensin on recovery from diet-induced milk fat depression.

The objective of the present experiment was to investigate the effect of monensin (MN) on the time course of recovery from diet-induced milk fat depression. Milk fat depression was induced in all cows (n = 16) during the first phase of each period by feeding a low-fiber, high-unsaturated fat diet [25.3% neutral detergent fiber (NDF), 6.9% fatty acids (FA), and 3.24% C18:2] with MN (450mg/cow per day) for 10 to 14d. A recovery phase of 18d followed, where cows were switched to a higher-fiber and lower unsaturated fat diet (31.2% NDF, 4.3% FA, and 1.7% C18:2). According to a crossover design, treatments during recovery were (1) control (no MN supplementation) or (2) continued MN supplementation. Milk yield, milk composition, and milk FA profile were measured every 3d during recovery. No effect was observed of MN on dry matter intake or yield of milk, milk protein, and lactose. Milk fat concentration and yield increased progressively during recovery in both treatments. Monensin decreased milk fat yield from d 6 to 15, but it was the same as the control on d 18. A treatment by time interaction on milk fat concentration was detected, which was decreased by MN only on d 3 and 6. The yield of milk de novo synthesized FA increased progressively in both treatments and was not affected by treatment. Similarly, yield of 16-C FA increased progressively, but was decreased by MN on d 6 and 9. Preformed FA yield was lower in the MN group from d 6 to 15, but was not different from the control on d 18. Importantly, milk FA concentration of trans-10 C18:1 and trans-10,cis-12 conjugated linoleic acid rapidly decreased in both groups; however, MN slightly increased trans-10 C18:1 concentration above baseline on d 15 and 18. In conclusion, MN supplementation had minimal effect on recovery of normal rumen biohydrogenation and de novo FA synthesis during recovery from milk fat depression by correction of dietary starch, NDF, and polyunsaturated FA concentration, but moderately decreased recovery of preformed FA in milk.