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Department of Animal Science, Cornell University, Ithaca, NY 14853
Corresponding author: D. E. Bauman; e-mail: deb6{at}cornell.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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Key Words: conjugated linoleic acid • early lactation • milk fat depression • net energy balance
Abbreviation key: CLA = conjugated linoleic acid, CLA-1 = low dose CLA treatment, CLA-2 = high dose CLA treatment, EE = ether extract, ME = metabolizable energy, MFD = milk fat depression, MP = metabolizable protein.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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An alternative approach to reduce the extent of negative energy balance is to decrease energy output during early lactation through temporary milk fat depression (MFD). Diet-induced MFD represents a situation where milk fat yield decreases without alteration of milk and milk protein yield. According to the biohydrogenation theory of MFD, the presence of unsaturated fatty acids from the diet and an altered rumen environment results in the formation of unique fatty acid intermediates that inhibit milk fat synthesis (Bauman and Griinari, 2003). One of these intermediates is trans-10, cis-12 CLA (Baumgard et al., 2000), and supplementation with rumen-protected CLA to pregnant, lactating cows for 20 wk promoted MFD with no apparent adverse effects (Perfield et al., 2002); therefore, it may constitute an efficient strategy to reduce milk energy output. Bernal-Santos et al. (2003) supplemented rumen-protected CLA to cows during the transition period, but no response was observed on milk fat percentage during the first 2 wk postpartum. Thereafter, CLA induced a reduction in milk fat content, but milk yield simultaneously increased so that there was no overall improvement in energy balance. Additionally, a more rapid return to estrous cycling was observed, but the number of animals was limited.
The objective of the present study was to evaluate the potential of 2 doses of rumen-protected CLA as an approach to reduce milk energy output in transition and early lactation cows, and this included effects on productive and reproductive performance.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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Supplements of Ca salts of palm fatty acid distillate and Ca salts of CLA contained 85 and 78% fat, respectively. The 3 supplements provided the same intake of fat (230 g/d) and were top-dressed once daily on the TMR from 21 d before expected day of calving to 63 DIM. The CLA-1 and CLA-2 treatments provided 31.6 and 63.2 g/d of CLA isomers, respectively. The 4 predominant CLA isomers in the supplements were trans-8, cis-10 (21.2%), cis-9, trans-11 (21.8%), trans-10, cis-12 (29.0%), and cis-11, trans-13 (28.0%). The predominant fatty acids in the Ca salts of palm fatty acid distillate were palmitic (42.6%), oleic (40.6%), and linoleic acids (10.1%).
Cows were fed TMR formulated using the Cornell Net Carbohydrate and Protein System (Fox et al., 2004). The diets for the prepartum period and the postpartum period are described in Table 1
, and all treatment groups received the same diet during these specific periods. The TMR samples were taken weekly, DM content was determined by drying at 54°C until a constant weight was reached, and then samples were composited at 4-wk intervals. Feed composites were analyzed by wet chemistry methods for CP, ADF, NDF, ether extract (EE), and minerals (Dairy One Cooperative Inc., Ithaca, NY), and values are reported in Table 1.
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After calving, cows were milked 3x /d, and milk weight was recorded. A milk sample from each milking was taken 1 d/wk, and a composite was formed based on proportion of daily yield. Composite milk samples were stored at 4°C with a preservative (bronopol tablet; D& F Control System, San Ramon, CA) until analyzed for fat, true protein, and lactose (Dairy One Cooperative Inc.) with the analytical and calibration methods described by Bernal-Santos et al. (2003). Additional aliquots of milk were taken, and a composite was formed during wk 1 to 6 postpartum. This composite was immediately frozen and stored at –20°C until analyzed for fatty acids.
Blood samples were taken at 10 and 5 d prepartum, 3x/wk during the first 11 wk of lactation, and once weekly from wk 12 to 18 postpartum. Blood (10 mL) was obtained via coccygeal venipuncture and was collected in vacuum tubes (Becton Dickinson Vacutainer Systems, Franklin Lakes, NJ) containing sodium heparin (100 U/mL of blood). Plasma was harvested within 20 min after collection by centrifugation (2800 x g for 15 min at 4°C) and stored at –20°C until metabolite and hormone analysis.
Liver samples were obtained via percutaneous trochar biopsy (Veenhuizen et al., 1991) on d 2 ± 1 and on d 21 ± 1 postpartum (mean ± SD). Liver samples were immediately frozen in liquid nitrogen and stored at – 80°C until analyzed for triglyceride content.
Estrus was synchronized with an intramuscular injection of 100 mg of GnRH analogue (Cystorelin; Abbott Laboratories, North Chicago, IL) at d 70 ± 3 (mean ± SD) postpartum; 7 d later, cows received an injection of 30 mg of PGF2
analogue (Lutalyse; Pharmacia & Upjohn, Kalamazoo, MI); 48 h later, they received an injection of 100 mg of GnRH and were inseminated 4 to 8 h later. Pregnancy was diagnosed by rectal palpation at 42 d after insemination. After the experimental period (>126 DIM), nonpregnant cows were resynchronized or inseminated when estrus was visually detected; if conception occurred before 185 d postpartum, this was recorded and used for statistical analysis.
A total of 46 of the 48 cows completed the treatment period. One cow from each CLA treatment group was excluded (all analysis) because of health reasons (chronic laminitis). In addition, 2 cows in the CLA-1 treatment group completed the treatment period but not the post-treatment period because of chronic laminitis and death caused by a respiratory problem.
Fatty Acid Analysis
The extraction and preparation of methyl esters of milk fatty acids was performed as described by Bernal-Santos et al. (2003). The fatty acid methyl esters were quantified using a gas chromatograph (Hewlett Packard HP6890; Wilmington, DE) equipped with a CP-Sil 88 capillary column (100 m x 0.25 mm i.d. with 0.2-µm film thickness; Varian Instruments, Walnut Creek, CA) under conditions as previously described by Perfield et al. (2002).
Lack of response in milk fat has been observed when Ca salts of CLA were fed several months after supplement manufacture (D. E. Bauman, unpublished data), and the cause appeared to be a polymerization of fatty acids that decreased the bioavailability and analytical detection of the CLA isomers (Asgeir Sæbø, Natural ASA, Hovdebydga, Norway; personal communication, 2002). In the present study, the fatty acid profile of the dietary supplements was analyzed monthly, and we observed a consistent CLA composition throughout the experiment. The analysis of the supplements was as described by Bernal-Santos et al. (2003) with gas chromatography procedures as described for milk fat.
Fatty acid peaks were identified using pure methyl ester standards (NuChek Prep, Elysian, MN). A butter oil reference standard (CRM 164; Commission of the European Community Bureau of References, Brussels, Belgium) was used to determine recovery factors for individual fatty acids and as a routine quality control.
Metabolite and Hormone Analysis
One plasma sample chosen from the end of each week was analyzed for NEFA and glucose. Plasma NEFA were quantified by enzymatic analysis (NEFA-C kit; Wako Chemicals, Richmond, VA) as previously described (Sechen et al., 1990). Glucose was determined by enzymatic analysis (procedure no. 510-A; Sigma Diagnostics, St. Louis, MO).
Plasma concentrations of progesterone and estradiol were determined by radioimmunoassay (Elrod and Butler, 1993; Beam and Butler, 1997). Progesterone was analyzed on the plasma samples obtained 3x/wk during the first 11 wk of lactation, whereas estradiol was analyzed on the plasma samples from the first 3 wk postpartum. Ovulation was determined based on temporal pattern and concentration of plasma progesterone according to the criteria described by Butler et al. (1981). Insulin was quantified by radioimmunoassay (McGuire et al., 1995) at wk 3, 6, and 9 postpartum using a composite sample formed from the 3 weekly plasma samples. Bovine insulin was used for iodination and standards (lot 615-70N-80; Lilly Research Laboratories, Greenfield, IN).
For triglyceride analysis, liver tissue was homogenized with a mixture of (2:1) chloroform:methanol, and lipid was extracted (Folch et al., 1957). Analysis of the extract involved a colorimetric method (Fletcher, 1968) with modifications described by Foster and Dunn (1973).
Statistical Analyses
Individual milk production and DMI values were reduced to weekly means before analysis, and the yields of fat, protein, and lactose were calculated using the weekly mean for milk production.
For all analysis, significance was declared at P < 0.05, and normality of residuals was verified for all ANOVA. Production variables, metabolites, and fatty acids were evaluated by ANOVA using the PROC MIXED procedure of SAS (2001) for repeated measures. The model included treatment, week of treatment, and cow within treatment as a random variable. When the interaction between treatment and week of treatment was significant (P < 0.05), this was also included. Blocking variables (lactation number and 305-d mature equivalent milk production in the previous lactation) were not significant, and, therefore, they were dropped from the model. Liver triglycerides were evaluated with PROC GLM of SAS, and the value from the first biopsy (d 2 ± 1) was used as a covariate for the second biopsy (d 21 ± 1).
Number of ovulations before synchronization and services per conception were analyzed using PROC GLM procedure of SAS (2001). Percentage of cows pregnant before 126 and 185 DIM, proportion of cows with estrogen-active follicles, and proportion of cows with ovulation in the first 21 d were analyzed with a 
2 test using PROC MIXED procedure of SAS (2001), where cow and treatment were class variables, and treatment was included in the model. For all analyses described previously, least squares means were calculated, and differences between treatments were detected with the Tukey’s adjustment.
Days to first ovulation and days to pregnancy were compared by survival analysis using PROC LIFETEST procedure of SAS (2001). Cows that did not ovulate before synchronization were censored (one cow from each treatment), as well as cows that did not become pregnant before 185 DIM (3 cows from CLA-1, 5 cows from CLA-2, and 8 cows from control group).
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RESULTS AND DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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). Relative to the control group, CLA supplements caused an average depression of 11 and 21% in milk fat yield over the 9-wk treatment period for CLA-1 and CLA-2, respectively (Table 2). The effect of CLA on milk fat was reversible, and treated groups returned to levels similar to the control when supplements were terminated (Figure 1). The reduction caused by CLA-1 was similar to that reported in the early lactation study by Bernal-Santos et al. (2003), where the Ca salts of CLA provided a similar dose of the trans-10, cis-12 CLA isomer. However, it is about one-half the magnitude of response reported by Perfield et al. (2002) for cows in established lactation; they observed a 23% reduction in milk fat yield over a 20-wk period when 8.8 g/d of trans-10, cis-12 were supplied as Ca salts.
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). In contrast, abomasal infusion of CLA resulted in an immediate decrease of milk fat during established lactation (Baumgard et al., 2000; Peterson et al., 2002), and supplementation with Ca salts of CLA caused MFD that reached nadir during the first week of treatment (Perfield et al., 2002). The trans-10, cis-12 CLA isomer was transferred to milk fat of CLA-supplemented cows at the first week postpartum in the present study (data not shown) and in previous work (Bernal-Santos et al., 2003). Therefore, the diminished response during the first weeks postpartum cannot be attributed to a limitation in mammary uptake of this CLA isomer. The cause is unknown, but may be due to a decrease in sensitivity or responsiveness of cows during early lactation, where many key enzymes and biochemical pathways are altered to support the onset of lactation (Bauman, 2000). Consistent with this, Moore et al. (2004) demonstrated a reduction in milk fat immediately postpartum when larger doses of trans-10, cis-12 CLA were used. They supplemented Ca salts of CLA at doses ranging from 12 to 37 g/d of trans-10, cis-12 CLA and observed a significant dose-dependent decrease in milk fat at 2 wk postpartum.
Experiments supplementing CLA in early lactation cows have often reported an increase in milk yield (Giesy et al., 1999; Bernal-Santos et al., 2003) and milk protein yield (Medeiros et al., 2000); however, this is not always observed. Milk yield, milk protein, and lactose were not affected by treatment in the present study (Table 2) or in other investigations during early lactation (Moore et al., 2004; Selberg et al., 2004). Results are consistent during established lactation where no increase in milk production or milk protein yield has been observed with CLA supplementation to cows fed TMR diets (Chouinard et al., 1999a,b; Baumgard et al., 2001; Perfield et al., 2002). A week x treatment interaction was observed in lactose percentage because of a lower value in the control group during the first week. This value might have been influenced by the presence of colostrum in one or more samples.
Energy, glucose, and amino acids can be limiting in early lactation (Oldham, 1984; Bell, 1995), and the difference in milk response between early lactation studies may be due to variation in nutrient availability. Based on this, the milk yield response in the early lactation studies has been attributed to the greater availability of energy caused by reduction of milk energy output in a physiological state where synthesis activity in the mammary gland is up-regulated (Bernal-Santos et al., 2003). The metabolizable energy (ME) and metabolizable protein (MP) balances over the first 9 wk postpartum in the study by Bernal-Santos et al. (2003) and the present study were determined using the Cornell Net Carbohydrate and Protein System (Fox et al., 2004). The diet in the present study provided a greater percentage of ME and MP requirements (92 vs. 86% and 96 vs. 88% for ME and MP, respectively). Compared with the study by Bernal-Santos et al. (2003), plasma NEFA concentrations for the control group during the first 8 wk postpartum were also lower during the same period (436 vs. 603 µM, respectively), consistent with the less extensive negative energy balance. Thus, nutrient status may influence whether the CLA-induced reduction in milk fat secretion results in a corresponding increase in milk yield.
Dietary supplements of CLA resulted in changes in the fatty acid composition of milk fat as shown for wk 6 postpartum (Table 3). Fatty acids can be grouped according to their origin: fatty acids synthesized de novo (<C16), fatty acids from the uptake of preformed fatty acids (>C16), and fatty acids from both sources (C16; McGuire and Bauman, 2002). The CLA-2 treatment slightly increased the proportion of preformed fatty acids and decreased the proportion of C16 in the milk. Fatty acids representing the product and substrate for 
9-desaturase were used to calculate the desaturase index, and there were no differences among treatments (Table 3). The small shifts in fatty acid composition and the lack of an effect on the desaturase index are comparable with the responses observed with abomasal infusion of low doses of CLA trans-10, cis-12 (<5 g/d; Baumgard et al., 2001; Peterson et al., 2002). This suggests that substantial metabolism of the Ca salts of CLA must have occurred in the rumen, so that the "effective dose" was much lower than the amount of CLA in the dietary supplement. Recently, de Veth et al. (2004) combined data from 7 studies in which cows were abomasally infused with trans-10, cis-12 CLA; they showed that the transfer of trans-10, cis-12 CLA to milk fat was linear across abomasal doses. Using this equation, we compared data in the present study, where the transfer of the trans-10, cis-12 CLA from the Ca salts to milk was 3.15 and 2.64% for CLA-1 and CLA-2, respectively. These values are equivalent to 12 and 14% of that expected with abomasal infusion of the same doses. Similar calculations comparing the transfer of trans-10, cis-12 CLA from dietary supplements to milk fat showed values of 15 and 22% of those expected with abomasal infusions for the established lactation study of Perfield et al. (2002) and the early lactation study of Bernal-Santos et al. (2003), respectively.
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). There was a treatment x week interaction for fatty acids <C16 and C16 (P < 0.05). In the cows supplemented with CLA-1, short-and medium-chain fatty acids (< C16) accounted for a smaller portion of the reduction during the first few weeks postpartum; however, the proportion increased gradually through the treatment period to where fatty acids < C16 accounted for >50% of the reduction (molar basis) at 6 wk postpartum (Figure 2, top panel). The reduction in fatty acids of cows supplemented with CLA-2 was more equally distributed among sources during the first 2 wk of lactation, but de novo synthesized fatty acids were also more extensively reduced after 3 wk postpartum (Figure 2, bottom panel). During early lactation, mammary uptake of preformed fatty acids is increased, and long-chain fatty acids represent a larger proportion of milk fatty acids (McGuire and Bauman, 2002). Thus, the greater reduction of pre-formed fatty acids observed with CLA supplements during the first weeks of lactation may be due to the fact that they contributed more extensively to milk fatty acids at the beginning of the lactation.
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). Further, DMI did not account for the difference because intake was similar among treatments (P = 0.35). Increased energy expenditure and fat oxidation have been reported in growing mice supplemented with CLA (West et al., 1998; Ohnuki et al., 2001), but the doses administered to mice are over 10-fold greater than the dose used in studies with lactating cows (Bauman et al., 2003). If increased energy expenditure occurs in cows, it will result in increased maintenance requirements and increased heat production. However, Shingfield et al. (2004) estimated energy balance of cows fed a control treatment or a rumen-protected CLA at wk 3, 7, 11, and 15 of lactation using excreta collection and respiration calorimetry. They observed increased yields of milk and milk protein, but did not find treatment differences in heat energy/BW0.75. In the present study, the net energy balance is an estimated value, and there were small numerical differences among treatments for each of the variables used in the calculations. Thus, the aggregation of these small differences may reflect the decrease in the energy expended for milk fat in CLA-treated cows. Further studies to clarify the bioenergetics of energy partitioning in lactating cows supplemented with CLA are needed.
Dietary supplements of CLA have been reported to cause insulin resistance in a few studies. Development of insulin resistance was reported in CLA-treated mice based on response to an insulin challenge, but no differences were observed in response to a glucose tolerance test (Tsuboyama-Kasaoka et al., 2000). Men supplemented with CLA for 12 wk also developed insulin resistance based on results from a euglycemic-hyperinsulinemic clamp, and this effect was attributed specifically to the trans-10, cis-12 isomer of CLA (Riserus et al., 2002a; Riserus et al., 2002b). In the present study, no differences among treatments were observed for plasma glucose or insulin (Table 4). Similarly, long-term studies in lactating cows observed no effect of CLA on plasma concentrations of glucose or insulin (Perfield et al., 2002; Bernal-Santos et al., 2003; Selberg et al., 2004). In addition, short-term studies in dairy cows established that CLA had no effect on plasma concentrations of glucose, insulin, or on the fractional rate of glucose clearance in response to insulin (Baumgard et al., 2000; Baumgard et al., 2002). Thus, at the doses of trans-10, cis-12 CLA that are affective in reducing milk fat secretion, there is no evidence of insulin resistance in the lactating cow.
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). This is in accordance with the results reported by Bernal-Santos et al. (2003) and Selberg et al. (2004) and suggests that CLA does not have an effect on hepatic fat accumulation in early lactation. Plasma concentrations of NEFA did not differ between treatments over the 9-wk treatment period (Table 4). However, the group supplemented with CLA-1 had a lower value during the first week postpartum (P <0.05) and tended to have lower plasma NEFA concentrations during the first 9 wk (Figure 3). Other studies in early and established lactation have not observed differences in NEFA caused by treatment with CLA (Perfield et al., 2002; Bernal-Santos et al., 2003; Moore et al., 2004). In contrast, Baumgard et al. (2002) observed a trend to decrease plasma NEFA concentrations after an epinephrine challenge in a short-term study (5 d), where cows were abomasally infused with 10 g/d of trans-10, cis-12 CLA.
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) are comparable with results reported in earlier studies that had similar numbers of animals (Medeiros et al., 2000; Bernal-Santos et al., 2003). Both of these earlier studies observed a trend for fewer days to first ovulation and a reduction in the number of days open for cows supplemented with CLA. In the present study, the median days to first ovulation was numerically lower for cows supplemented with CLA-1. There was a trend (P = 0.07) for the proportion of cows pregnant before 185 d to differ among treatments, with the highest value observed for the CLA-1 group (Table 5). The percentage of cows pregnant before 126 DIM of the 2 CLA groups was similar (31.1 and 33.3%) and numerically greater than the control group (18.7%).
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(Mattos et al., 2000). The inhibition of PGF2 can decrease embryonic loss by avoiding luteolysis when maternal recognition of pregnancy does not occur (Abayasekara and Wathes, 1999). Conjugated linoleic acid has been reported to have an effect on prostaglandin synthesis in several different species and cell systems (Belury, 2002). Of special interest is the inhibition of PGF2 observed in uterine tissue of pregnant rats supplemented with CLA (Harris et al., 2001) and the decreased production of PGF2 in endometrial cells incubated with CLA (Cheng et al., 2003). Large-scale field studies will be required to establish more clearly the effect of CLA in reproduction.
Production-related variables for the post-treatment period are presented in Table 6. No differences were observed in milk production or milk components because of treatment. There was a significant treatment x week interaction for milk and milk lactose yields, and this was due to slightly greater yields in the CLA-2 group for wk 1 to 3 post-treatment. Milk fat depression was reversible, and milk fat content of the CLA groups returned to levels similar to the control group when the CLA supplement was terminated (Figure 1). This is in accordance with the temporal pattern observed in short-term studies with abomasal infusions of CLA (Chouinard et al., 1999a,b; Baumgard et al., 2000). Thus, the present study shows that CLA may be supplemented for the first 9 wk postpartum without any post-treatment effects.
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CONCLUSIONS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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Further studies are needed to clarify the partitioning of energy in CLA-supplemented cows. Of particular interest is the use of the energy spared by the reduction in milk fat with CLA supplementation in early lactation and to elucidate the basis for the variability in the response in milk yield seen in other studies. Additionally, large-scale studies are necessary to establish definitively the effects of dietary CLA supplements on reproduction of dairy cows.
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ACKNOWLEDGEMENTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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FOOTNOTES |
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Received for publication June 8, 2004. Accepted for publication November 15, 2004.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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