Subcutaneous lysophosphatidylcholine administration promotes a febrile and immune response in Holstein heifer calves.

Lysophosphatidylcholine (LPC) is immunomodulatory in nonruminants; however, the actions of LPC on immunity in cattle are undefined. Our objective was to study the effects of LPC administration on measures of immunity, liver health, and growth in calves. Healthy Holstein heifer calves (n = 46; age 7 ± 3 d) were randomly assigned to 1 of 4 treatments (n = 10 to 11 calves/treatment): a milk replacer diet unsupplemented with lecithin in the absence (CON) or presence of subcutaneously (s.c.) administered mixed (mLPC; 69% LPC-16:0, 25% LPC-18:0, 6% other) or pure LPC (pLPC; 99% LPC-18:0), or a milk replacer diet supplemented with 3% lecithin enriched in lysophospholipids containing LPC in the absence of s.c.-administered LPC (LYSO) for 5 wk. Calves received 5 s.c. injections of vehicle (10 mL of phosphate-buffered saline containing 20 mg of bovine serum albumin/mL; CON and LYSO) or vehicle containing mLPC or pLPC to provide 10 mg of total LPC per kilogram of BW per injection every 12 h during wk 2 of life. Calves were fed a milk replacer containing 27% crude protein and 24% fat at 1.75% of BW per day (dry matter basis) until wk 6 of life (start of weaning). Starter grain and water were provided ad libitum. Body measurements were recorded weekly, and clinical observations were recorded daily. Blood samples were collected weekly before morning feeding and at 0, 5, and 10 h, relative to the final s.c. injection of vehicle or LPC. Data were analyzed using a mixed model, with repeated measures including fixed effects of treatment, time, and their interaction. Dunnett's test was used to compare treatments to CON. Peak rectal temperatures were higher in mLPC or pLPC, relative to CON. Plasma LPC concentrations were greater in mLPC and LYSO calves 5 h and 10 h after the final injection, relative to CON. Calves receiving mLPC and pLPC also had higher circulating serum amyloid A concentrations, relative to CON. Calves receiving mLPC had greater serum aspartate aminotransferase, γ-glutamyltransferase, and glutamate dehydrogenase concentrations, relative to CON. Calves provided mLPC experienced lower average daily gain (ADG) after weaning, relative to CON. The LYSO treatment did not modify rectal temperatures, ADG, or measures of liver health, relative to CON. We conclude that LPC administered as s.c. injections induced an acute febrile response, modified measures of liver and immune function, and impaired growth in calves.

Effects of dietary organic acid and pure botanical supplementation on growth performance and circulating measures of metabolic health in Holstein calves challenged by heat stress.

To evaluate the effects of heat stress environmental conditioning and dietary supplementation with organic acid and pure botanicals (OA/PB) on growth in dairy calves, we enrolled 62 bull (noncastrated) and heifer calves in a study with a completely randomized design. Calves were assigned to 1 of 5 groups (n = 11 to 14/group): (1) thermoneutral conditions (TN-Con), (2) HS conditions (HS-Con), (3) thermoneutral conditions and pair-fed to match nutrient intake with HS-Con (TN-PF), (4) HS with low-dose OA/PB [75 mg/kg of body weight (BW); 25% citric acid, 16.7% sorbic acid, 1.7% thymol, 1.0% vanillin, and 55.6% triglyceride; HS-Low], or (5) HS with high-dose OA/PB (150 mg/kg of BW; HS-High). Supplements were delivered as a twice-daily bolus via the esophagus from wk 1 through 13 of life; all calves, including those on the control treatments, received an equivalent amount of triglyceride used for microencapsulation. Calves were raised in TN conditions from birth until weaning. After weaning, calves (62 ± 2 d; 91 ± 10.9 kg of BW) were transported to a new facility and remained in TN conditions [temperature-humidity index (THI): 60 to 69] for a 7-d covariate period. Thereafter, calves remained in TN or were moved to HS conditions (THI: diurnal change 75 to 83 during night and day, respectively) for 19 d. Clinical assessments were performed thrice daily, BW was recorded weekly, and blood was sampled on d 1, 2, 3, 8, 15, and 19. Upon experiment completion, calves from HS-Con and TN-Con were euthanized, and hot carcass and visceral organ weights were recorded. The mixed model included calf as a random effect; treatment, day, hour (when appropriate) as fixed effects, and the interactions of treatment × day and treatment × hour (when appropriate). Rectal and skin temperatures and respiration rates were greater in HS-Con than in TN-Con. During heat stress exposure, dry matter intake (DMI), average daily gain (ADG), and gain to feed (G:F) were lower in HS-Con relative to TN-Con. Comparing HS-Con and TN-PF, ADG and G:F were similar. Plasma fatty acid concentrations were elevated in TN-PF compared with HS-Con and TN-Con. Despite tendencies for increased aspartate aminotransferase, HS conditions did not overtly influence liver and inflammation markers. Liver weights were lower in HS-Con relative to TN-Con. During the first week of heat exposure, DMI was greater for HS-Low relative to HS-Con. Supplementation of OA/PB at low and high levels had a similar G:F to HS-Con. We conclude that reductions in DMI accounted for production losses during HS conditioning and that dietary OA/PB supplementation was not able to improve growth performance in heat-stressed calves.

Heat stress develops with increased total-tract gut permeability, and dietary organic acid and pure botanical supplementation partly restores lactation performance in Holstein dairy cows.

To evaluate the effects of heat stress (HS) conditions and dietary organic acid and pure botanical (OA/PB) supplementation on gut permeability and milk production, we enrolled 46 multiparous Holstein cows [208 ± 4.65 dry matter intake (DMI; mean ± SD), 3.0 ± 0.42 lactation, 122 ± 4.92 d pregnant, and 39.2 ± 0.26 kg of milk yield] in a study with a completely randomized design. Cows were assigned to 1 of 4 groups: thermoneutral conditions (TN-Con, n = 12), HS conditions (HS-Con, n = 12), thermoneutral conditions pair-fed to HS-Con (TN-PF, n = 12), or HS supplemented with OA/PB [75 mg/kg of body weight (BW); 25% citric acid, 16.7% sorbic acid, 1.7% thymol, 1.0% vanillin, and 55.6% triglyceride; HS-OAPB, n = 10]. Supplements were delivered twice daily by top-dress; all cows not supplemented with OA/PB received an equivalent amount of the triglyceride used for microencapsulation of the OA/PB supplement as a top-dress. Cows were maintained in thermoneutrality [temperature-humidity index (THI) = 68] during a 7-d acclimation and covariate period. Thereafter, cows remained in thermoneutral conditions or were moved to HS conditions (THI: diurnal change 74 to 82) for 14 d. Cows were milked twice daily. Clinical assessments and BW were recorded, blood was sampled, and gastrointestinal permeability measurements were repeatedly evaluated. The mixed model included fixed effects of treatment, time, and their interaction. Rectal and skin temperatures and respiration rates were greater in HS-Con and HS-OAPB relative to TN-Con. Dry matter intake, water intake, and yields of energy-corrected milk (ECM), protein, and lactose were lower in HS-Con relative to HS-OAPB. Nitrogen efficiency was improved in HS-OAPB relative to HS-Con. Compared with TN-Con and TN-PF, milk yield and ECM were lower in HS-Con cows. Total-tract gastrointestinal permeability measured at d 3 of treatment was greater in HS-Con relative to TN-Con or TN-PF. Plasma total fatty acid concentrations were reduced, whereas insulin concentrations were increased in HS-Con relative to TN-PF. We conclude that exposure to a heat-stress environment increases total-tract gastrointestinal permeability. This study highlights important mechanisms that might account for milk production losses caused by heat stress, independent of changes in DMI. Our observations also suggest that dietary supplementation of OA/PB is a means to partly restore ECM production and improve nitrogen efficiency in dairy cattle experiencing heat stress.

Effects of abomasal infusions of fatty acids and 1-carbon donors on apparent fatty acid digestibility and incorporation into milk fat in cows.

Our primary objective was to determine the effects of the abomasal infusion of 16-carbon (16C) and 22-carbon (22C) fatty acids (FA) on apparent FA digestibility, plasma FA concentrations, and their incorporation into milk fat in cows. Our secondary objective was to study the effects of 1-carbon donors choline and l-serine on these variables. Five rumen-cannulated Holstein cows (214 ± 4.9 d in milk; 3.2 ± 1.1 parity) were enrolled in a 5 × 5 Latin square experiment with experimental periods lasting 6 d. Abomasal infusates consisted of (1) palmitic acid (PA; 98% 16:0 of total fat), (2) PA + choline chloride (PA+CC; 50 g/d of choline chloride), (3) PA + l-serine (PA+S; 170 g/d of l-serine), (4) behenic acid (BA; 92% 22:0 of total fat), and (5) docosahexaenoic acid algal oil (DHA; 47.5% DHA of total fat). Emulsions were formulated to provide 301 g/d of total FA and were balanced to provide a minimum of 40 and 19 g/d of 16:0 and glycerol, respectively, to match the content found in the infused algal oil. Apparent digestibility of FA was highest in DHA, intermediate in PA, and lowest in BA. Digestibility of 16C FA was lowest in BA and highest in PA. The digestibility of 22C FA was highest in DHA relative to BA (99 vs. 58%), whereas 1-carbon donors had no effect on 22C FA digestibility. Plasma 16C FA concentrations were greatest with PA treatment, and 22C FA concentrations were ~3-fold greater in DHA-treated cows relative to all other treatments. Milk fat 16:0 content was highest in PA relative to BA and DHA (e.g., 37 vs. 27% in PA and DHA), whereas the milk yield of 16:0 was higher in PA relative to DHA (i.e., 454 vs. 235 g/d). Similarly, milk 22:0 content and yield were ~10-fold higher in BA relative to all other treatments, whereas DHA treatment resulted in higher content and yield of 22:6 in milk fat relative to all other treatments (41- and 38-fold higher, respectively). Consequently, the content of FA >16C (i.e., preformed) was higher in milk fat from cows infused with BA and DHA relative to PA. De novo FA content in milk did not differ between PA, PA+CC, and PA+S (~16% of milk fat) but was higher in BA and DHA treatments (19 and 21%, respectively). We conclude that FA carbon chain length and degree of saturation affected FA digestibility and availability for absorption as well as their incorporation into milk fat. The abomasal infusion of choline chloride and l-serine did not modify these variables relative to infusing palmitic acid alone.

Effects of dietary deoiled soy lecithin supplementation on milk production and fatty acid digestibility in Holstein dairy cows.

Deoiled soy lecithin is a feed additive enriched in phospholipids. Our study evaluated the effects of dietary deoiled soy lecithin supplementation on (1) milk production and composition, (2) plasma and milk fatty acid (FA) content and yield, and (3) apparent FA digestibility and absorption in lactating dairy cows fed fractionated palm fat. In a split-plot Latin square design, 16 Holstein cows (160 ± 7 days in milk; 3.6 ± 1.2 parity) were randomly allocated to a main plot receiving a corn silage and alfalfa haylage-based diet with palm fat containing either moderate (MPA) or high palmitic acid (HPA) content at 1.75% of ration dry matter (72 or 99% palmitic acid, respectively; n = 8/palm fat diet). On each palm fat diet, deoiled soy lecithin was top-dressed at 0, 0.12, 0.24, or 0.36% of ration dry matter in a replicated 4 × 4 Latin square design. Following a 14-d covariate period, lecithin supplementation spanned 14 d, with milk and blood collected during the final 3 d. Milk composition and pooled plasma markers were measured. The statistical model included the fixed effects of palm fat type, lecithin dose, period, and the interaction between palm fat type and lecithin dose. The random effect of cow nested within palm fat group was also included. Lecithin linearly decreased dry matter intake. In cows fed HPA, lecithin feeding reduced milk fat content and tended to decrease milk fat yield. Although no changes in milk yield were observed, a quadratic reduction in 3.5% fat-corrected milk was observed with increasing lecithin dose. Lecithin linearly increased energy-corrected milk efficiency in cows fed MPA. Lecithin supplementation also decreased milk urea nitrogen, relative to unsupplemented cows. The proportion of 16-carbon FA in milk fat decreased linearly with lecithin dose, whereas 18-carbon FA increased linearly. Lecithin reduced de novo FA (<16-carbon) content and tended to increase preformed FA (>16-carbon) content in a linear manner. Compared with MPA, HPA diets reduced apparent total and 16-carbon FA digestibility and absorption. Deoiled soy lecithin feeding did not modify FA digestibility or absorption. Our observations suggest that soy lecithin feeding modifies rumen digestion to reduce dry matter intake and change milk composition.

Short communication: Effects of dietary deoiled soy lecithin supplementation on circulating choline and choline metabolites, and the plasma phospholipid profile in Holstein cows fed palm fat.

Dietary lecithin is a source of choline. Our objective was to evaluate the effects of dietary deoiled soy lecithin feeding on circulating choline, choline metabolites, and the plasma phospholipid profile in lactating dairy cows fed fractionated palm fatty acids. In a split-plot Latin square design, 16 Holstein cows (160 ± 7 d in milk; 3.6 ± 1.2 parity) were randomly allocated to a main plot receiving a corn silage and alfalfa haylage-based diet with palm fat containing either moderate or high palmitic acid content at 1.75% of ration dry matter (moderate and high palmitic acid containing 72 or 99% palmitic acid in fat supplement, respectively; n = 8/palm fat diet). Within each palm fat group, deoiled soy lecithin was top-dressed at 0, 0.12, 0.24, or 0.36% of ration dry matter in a replicated 4 × 4 Latin square design with 14-d experimental periods. A 14-d covariate period was used to acclimate cows to palm fat feeding without lecithin supplementation. Blood sampling occurred during the final 3 d of each experimental period. Plasma choline and choline metabolites were quantified using liquid chromatography and mass spectrometry. Plasma phospholipids were profiled using time-of-flight mass spectrometry. Whereas no effects of treatments were detected for plasma choline or methionine, lecithin feeding increased the plasma concentrations of choline metabolites trimethylamine N-oxide and dimethylglycine (24 and 11%, respectively). Plasma phosphatidylcholine (PC) and sphingomyelin (SM) concentrations increased with deoiled lecithin feeding (e.g., PC 16:0/22:6 and SM d18:1/18:3). Lecithin supplementation also increased plasma lysophosphatidylcholine (LPC) concentrations (e.g., LPC 18:0) while reducing plasma phosphatidylethanolamine (PE) concentrations (e.g., PE 16:0/20:5). Although increases in microbial-derived trimethylamine N-oxide suggest gastrointestinal lecithin degradation, elevations in plasma dimethylglycine, PC, LPC, and SM suggest that choline availability was improved by lecithin feeding in cows, thus supporting enhanced endogenous phospholipid synthesis.

Symposium review: One-carbon metabolism and methyl donor nutrition in the dairy cow.

The present review focuses on methyl donor metabolism and nutrition in the periparturient and lactating dairy cow. Methyl donors are involved in one-carbon metabolism, which includes the folate and Met cycles. These cycles work in unison to support lipid, nucleotide, and protein synthesis, as well as methylation reactions and the maintenance of redox status. A key feature of one-carbon metabolism is the multi-step conversion of tetrahydrofolate to 5-methyltetrahyrofolate. Homocysteine and 5-methyltetrahyrofolate are utilized by vitamin B12-dependent Met synthase to couple the folate and Met cycles and generate Met. Methionine may also be remethylated from choline-derived betaine under the action of betaine hydroxymethyltransferase. Regardless, Met is converted within the Met cycle to S-adenosylmethionine, which is universally utilized in methyl-group transfer reactions including the synthesis of phosphatidylcholine. Homocysteine may also enter the transsulfuration pathway to generate glutathione or taurine for scavenging of reactive oxygen metabolites. In the transition cow, a high demand exists for compounds with a labile methyl group. Limited methyl group supply may contribute to inadequate hepatic phosphatidylcholine synthesis and hepatic triglyceride export, systemic oxidative stress, and compromised milk production. To minimize the perils associated with methyl donor deficiency, the peripartum cow relies on de novo methylneogenesis from tetrahydrofolate. In addition, dietary supplementation of rumen-protected folic acid, vitamin B12, Met, choline, and betaine are potential nutritional approaches to target one-carbon pools and improve methyl donor balance in transition cows. Such strategies have merit considering research demonstrating their ability to improve milk production efficiency, milk protein synthesis, hepatic health, and immune response. This review aims to summarize the current understanding of folic acid, vitamin B12, Met, choline, and betaine utilization in the dairy cow. Methyl donor co-supplementation, fatty acid feeding strategies that may optimize methyl donor supplementation efficacy, and potential epigenetic mechanisms are also considered.

Methyl donor supplementation suppresses the progression of liver lipid accumulation while modifying the plasma triacylglycerol lipidome in periparturient Holstein dairy cows.

Co-supplementation of methyl donors may lower hepatic lipid content in transition cows. To define the ability of methyl donor supplementation (MDS) to reduce hepatic lipid content and modify the plasma lipidome, 30 multiparous Holstein cows (2.04 ± 0.69 lactations; 689 ± 58 kg of body weight; 3.48 ± 0.10 units of body condition score) were fed a ration with or without rumen-protected methyl donors (22 g/d of Met, 10 g/d of choline chloride, 3 g/d of betaine, 96 mg/d of riboflavin, and 1.4 mg/d of vitamin B12) from d -28 before expected calving through d 14 postpartum. Cows were randomly enrolled based on predefined selection criteria (body condition score and parity). Base diets without MDS were formulated for gestation (15.4% crude protein with a predicted Lys-to-Met ratio of 3.25; 1.44 Mcal of net energy for lactation/kg of dry matter) and lactation (16.6% crude protein with a predicted Lys-to-Met ratio of 3.36; 1.64 Mcal of net energy for lactation/kg of dry matter). Blood sampling occurred from d -28 relative to expected calving through d 14 postpartum. Liver tissue was biopsied at d -28 relative to expected calving and on d 5 and 14 postpartum. In addition to routine analyses, serum AA concentrations on d 10 and 12 were quantified using mass spectrometry. Plasma triacylglycerol (TAG) and cholesteryl esters (CE) were qualitatively measured using time-of-flight mass spectrometry. Data were analyzed using a mixed model with repeated measures. Dry matter intake and milk yield were not modified by MDS. The transition from d -28 relative to expected parturition to d 14 postpartum was characterized by increased plasma fatty acid (0.15 to 0.71 mmol/L) and ß-hydroxybutyrate (0.34 to 0.43 mmol/L) levels and liver lipid content (3.91 to 9.16%). Methyl donor supplementation increased the serum Met level by 26% and decreased the serum Lys-to-Met ratio by 21% on d 10 and 12, respectively. Moreover, the increase in hepatic lipid content from d 5 through 14 postpartum was suppressed with MDS relative to control (3.57 vs. -0.29%). Dietary MDS modified the TAG and CE lipidome. For example, MDS increased plasma TAG 46:3 (carbon number:double bond) by 116% relative to control cows on d 5 postpartum. Moreover, MDS tended to increase plasma CE 34:6. In contrast, MDS lowered plasma TAG 54:8 by 39% relative to control cows on d 5 postpartum. We concluded that in the absence of gains in dry matter intake and milk and milk protein yields, dietary MDS slows the progression of hepatic lipid accumulation and modifies the plasma TAG lipidome in transition cows.

Increasing palmitic acid intake enhances milk production and prevents glucose-stimulated fatty acid disappearance without modifying systemic glucose tolerance in mid-lactation dairy cows.

Feeding saturated fatty acids may enhance milk yield in part by decreasing insulin sensitivity and shifting glucose utilization toward the mammary gland. Our objective was to evaluate the effects of palmitic acid (C16:0) on milk production and insulin sensitivity in cows. Twenty multiparous mid-lactation Holstein cows were enrolled in a study consisting of a 5-d covariate, 49-d treatment, and 14-d posttreatment period. All cows received a common sorghum silage-based diet and were randomly assigned to a diet containing no supplemental fat (control; n=10; 138±45d in milk) or C16:0 at 4% of ration DM (PALM; 98% C16:0; n=10; 136±44d in milk). Blood and milk were collected at routine intervals. Intravenous glucose tolerance tests (300mg/kg of body weight) were performed at d -1, 24, and 49 relative to start of treatment. Data were analyzed as repeated measures using a mixed model with fixed effects of treatment and time, and milk yield served as a covariate. The PALM treatment increased milk yield by wk 7. Furthermore, PALM increased milk fat yield and energy-corrected milk at wk 3 and 7. Changes in milk production occurred in parallel with enhanced energy intake. Increased milk fat yield during PALM treatment was due to increased C16:0 and C16:1 incorporation; PALM had no effect on concentration of milk components, BW, or body condition score. Two weeks posttreatment, energy-corrected milk and milk fat yield remained elevated in PALM-fed cows whereas yields of milk were similar between treatments. Increased milk fat yield after PALM treatment was due to increased de novo lipogenesis and uptake of preformed fatty acids. The basal concentration of nonesterified fatty acids (NEFA) in plasma increased by d 4, 6, and 8 of PALM treatment, a response not observed thereafter. Although PALM supplementation did not modify insulin, glucose, or triacylglycerol levels in plasma, total cholesterol in plasma was elevated by wk 3. Estimated insulin sensitivity was lower during the first week of PALM treatment; however, glucose disposal following glucose tolerance tests was not modified. In contrast, C16:0 feeding reduced glucose-stimulated NEFA disappearance by wk 7. Results demonstrate that increasing dietary energy from C16:0 for 7wk improves milk yield and milk composition without modifying systemic glucose tolerance. Reduced glucose-stimulated NEFA disappearance with C16:0 feeding and elevated circulating NEFA may reflect changes in adipose tissue insulin sensitivity.

Palmitic acid feeding increases ceramide supply in association with increased milk yield, circulating nonesterified fatty acids, and adipose tissue responsiveness to a glucose challenge.

Reduced insulin action is a key adaptation that facilitates glucose partitioning to the mammary gland for milk synthesis and enhances adipose tissue lipolysis during early lactation. The progressive recovery of insulin sensitivity as cows advance toward late lactation is accompanied by reductions in circulating nonesterified fatty acids (NEFA) and milk yield. Because palmitic acid can promote insulin resistance in monogastrics through sphingolipid ceramide-dependent mechanisms, palmitic acid (C16:0) feeding may enhance milk production by restoring homeorhetic responses. We hypothesized that feeding C16:0 to mid-lactation cows would enhance ceramide supply and ceramide would be positively associated with milk yield. Twenty multiparous mid-lactation Holstein cows were enrolled in a study consisting of a 5-d covariate, 49-d treatment, and 14-d posttreatment period. All cows were randomly assigned to a sorghum silage-based diet containing no supplemental fat (control; n=10; 138±45 d in milk) or C16:0 at 4% of ration dry matter (PALM; 98% C16:0; n=10; 136±44 d in milk). Blood and milk were collected at routine intervals. Liver and skeletal muscle tissue were biopsied at d 47 of treatment. Intravenous glucose tolerance tests (300mg/kg of body weight) were performed at d -1, 24, and 49 relative to start of treatment. The plasma and tissue concentrations of ceramide and glycosylated ceramide were determined using liquid chromatography coupled with tandem mass spectrometry. Data were analyzed as repeated measures using a mixed model with fixed effects of treatment and time, and milk yield served as a covariate. The PALM treatment increased milk yield, energy-corrected milk, and milk fat yield. The most abundant plasma and tissue sphingolipids detected were C24:0-ceramide, C24:0-monohexosylceramide (GlcCer), and C16:0-lactosylceramide. Plasma concentrations of total ceramide and GlcCer decreased as lactation advanced, and ceramide and GlcCer were elevated in cows fed PALM. Palmitic acid feeding increased hepatic ceramide levels, a response not observed in skeletal muscle tissue. Plasma ceramides (e.g., C24:0-ceramide) were positively correlated with plasma NEFA and milk yield, and positively correlated with NEFA levels following a glucose challenge. Our data demonstrate a remodeled plasma and hepatic sphingolipidome in mid-lactation dairy cows fed PALM. The potential involvement in ceramide in homeorhetic nutrient partitioning to support lactation requires further consideration.

Effects of intravenous infusion of trans-10, cis-12 18:2 on mammary lipid metabolism in lactating dairy cows.

It has previously been established that supplementation of trans-10, cis-12 18:2 reduces milk fat content and fat deposition in several species. The objectives of the study were 1) to examine whether potential mechanisms by which trans-10, cis-12 18:2 is reported to affect lipid metabolism in adipose tissue of different species could be partly responsible for the inhibition in milk fat synthesis in lactating dairy cows; and 2) to investigate the effects of trans-10, cis-12 18:2 on the expression of a newly identified isoform of stearoyl-coenzyme A desaturase (SCD) in bovine mammary tissue. Four primiparous Holstein cows in established lactation, fitted with indwelling jugular catheters, were used in a balanced 2 x 2 crossover design. For the first 5 d of each period, cows were infused intravenously with a 15% lipid emulsion providing 10 g/d of either cis-9, cis-12 18:2 (control) or trans-10, cis-12 18:2 (conjugated linoleic acid; CLA). On d 5 of infusion, mammary gland biopsies were performed and tissues were analyzed for mRNA expression of acetyl-coenzyme A carboxylase, fatty acid synthetase, lipoprotein lipase, SCD1, SCD5, sterol regulatory element-binding protein-1, IL6, IL8, and tumor necrosis factor-alpha by real-time PCR. Compared with the control treatment, CLA reduced milk fat concentration and yield by 46 and 38%, respectively, and increased the trans-10, cis-12 18:2 content in milk fat from 0.05 to 3.54 mg/g. Milk yield, milk protein, and dry matter intake were unaffected by treatment. Infusion of the CLA treatment reduced the mRNA expression of acetyl-coenzyme A carboxylase and fatty acid synthetase by 46 and 57%, respectively, and tended to reduce the expression of SCD1 and lipoprotein lipase. Abundance of mRNA for sterol regulatory element-binding protein-1 was reduced by 59% in the CLA treatment group. However, infusing trans-10, cis-12 18:2 did not affect the expression of transcripts for SCD5, tumor necrosis factor-alpha, IL6, and IL8. Results from the current study corroborate the idea that effects of trans-10, cis-12 18:2 reported on adipose tissue in animal models and humans are not part of the response in the inhibition of milk fat synthesis in lactating dairy cows. They also support the hypothesis that SCD1 and SCD5 present important differences in their regulation and physiological roles.

Dietary L-carnitine affects periparturient nutrient metabolism and lactation in multiparous cows.

The objectives of this study were to determine the effects of dietary L-carnitine supplementation on liver lipid accumulation, hepatic nutrient metabolism, and lactation in multiparous cows during the periparturient period. Cows were assigned to treatments at d -25 relative to expected calving date and remained on the experiment until 56 d in milk. Treatments were 4 amounts of supplemental dietary carnitine: control (0 g/d of L-carnitine; n = 14); low carnitine (LC, 6 g/d; n = 11); medium carnitine (MC, 50 g/d; n = 12); and high carnitine (HC, 100 g/d; n = 12). Carnitine was supplied by mixing a feed-grade carnitine supplement with 113.5 g of ground corn and 113.5 g of dried molasses, which was then fed twice daily as a topdress to achieve desired daily carnitine intakes. Carnitine supplementation began on d -14 relative to expected calving and continued until 21 d in milk. Liver and muscle carnitine concentrations were markedly increased by MC and HC treatments. Milk carnitine concentrations were elevated by all amounts of carnitine supplementation, but were greater for MC and HC than for LC during wk 2 of lactation. Dry matter intake and milk yield were decreased by the HC treatment. The MC and HC treatments increased milk fat concentration, although milk fat yield was unaffected. All carnitine treatments decreased liver total lipid and triacylglycerol accumulation on d 10 after calving. In addition, carnitine-supplemented cows had higher liver glycogen during early lactation. In general, carnitine supplementation increased in vitro palmitate beta-oxidation by liver slices, with MC and HC treatments affecting in vitro palmitate metabolism more potently than did LC. In vitro conversion of Ala to glucose by liver slices was increased by carnitine supplementation independent of dose. The concentration of nonesterified fatty acids in serum was not affected by carnitine. As a result of greater hepatic fatty acid beta-oxidation, plasma beta-hydroxybutyric acid was higher for the MC and HC treatments. Serum insulin was greater for all carnitine treatments, although plasma glucose was unaffected. Plasma urea N was lower and plasma total protein was higher for the MC and HC treatments. By decreasing liver lipid accumulation and stimulating hepatic glucose output, carnitine supplementation might improve glucose status and diminish the risk of developing metabolic disorders during early lactation.