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1 Department of Animal Science, P.O. Box 28, 00014 University of Helsinki, Finland
2 Department of Clinical Veterinary Medicine, University of Helsinki, Pohjoinen pikatie 800, 04920 Saarentaus, Finland
3 Herbivore Research Unit, INRA, Theix-63122, St-Genes Champanelle, France
Corresponding author: Tuomo Kokkonen; e-mail: tuomo.kokkonen{at}helsinki.fi.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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Key Words: dairy cow • body fatness • lipid mobilization • leptin
Abbreviation key: 3-MH = 3-methylhistidine, C = control group, EB = energy balance, ECM = energy-corrected milk yield, FD = fat depth, G0 = no glucogenic supplement, G1 = with glucogenic supplement, ME = metabolizable energy, T = test group.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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The supply of glucose precursors affects the fate of fatty acids in liver. When the supply of propionate, glucogenic amino acids, lactate, and glycerol decreases, a greater proportion of acetyl coenzyme A ends up in ketogenesis as a glucose-sparing mechanism (Rukkwamsuk et al., 1999). Decreased feed intake and thereby lowered propionate production in the rumen, in connection with increased NEFA supply to the liver, probably accounts for the increased risk of ketosis in overconditioned cows (Rukkwamsuk et al., 1999). Glucogenic supplementation may decrease ketone formation directly by increasing complete oxidation of NEFA or indirectly by decreasing mobilization of NEFA via elevated blood insulin or increased fatty acid re-esterification in adipose tissue (Burhans and Bell, 1998).
Bell et al. (2000) suggested that a high-yielding dairy cow might mobilize as much as 1000 g of tissue protein per day for the first 7 to 10 d of lactation. In underfed dairy cows, protein mobilization from skeletal muscles may account for 50% of the total protein mobilization (Chilliard and Robelin, 1983). The net contribution of amino acid mobilization to glucose production is considerably smaller than total mobilization as a result of increased milk protein synthesis, and increases in protein synthesis in the liver and digestive tract may mask, in part, mobilization of amino acids from muscles (Chilliard, 1999).
Several hormones control metabolic adaptation during the transition period. Based on the evidence from other species (human, rat, sheep), leptin may play an important role during this adaptation period by coordinating feed intake, energy expenditure, and tissue nutrient use (Ingvartsen and Boisclair, 2001). Leptin may have an autocrine/paracrine effect on inhibition of lipogenesis and stimulation of lipolysis. The degree of body fatness explains a large part of the variation in plasma leptin concentrations in sheep and cattle (Chilliard et al., 2001). Block et al. (2001) reported that the decrease in plasma leptin near parturition coincides with the onset of negative energy balance (EB) induced by the initiation of copious milk secretion.
The objective of the present experiment was to study the effects of body fatness on lipid and amino acid mobilization and on plasma leptin concentrations. Furthermore, we studied the lipolytic response of adipose tissue during the periparturient period. We also studied the effect of glucogenic supplementation on tissue mobilization and ketogenesis.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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The deliberate allocation of cows with the highest BCS within each block to the T group was based on the assumption that relatively more nutrients are deposited in tissues during late lactation than during the dry period, and that initial differences in body fatness were due to differences in feed intake during late lactation. Our aim was to scale up the differences between fatter and thinner cows. However, it must be noted that higher initial BCS may include a genetic predisposition toward fatness in addition to differing nutritional histories of the animals.
Feeds and Feeding
The feeding plan is summarized in Table 1
. Between d 56 and 21 prepartum, the cows in group C were fed individually according to energy recommendations (Tuori et al., 2000). The metabolizable energy (ME) requirement for maintenance was calculated according to MAFF (1975): (8.3 + 0.091 x BW) and an additional allowance of 18.7 MJ/d was made for pregnancy. The target ME allowance for cows in group T was 34 MJ/d over the MAFF recommendation. The additional energy is equivalent to the requirement for 1 kg/d BW gain (MAFF, 1975). Average feed allowances and chemical composition of the diets between d 56 and 21 prepartum are shown in Table 2. Based on feed analyses, the actual difference in ME allowances (38 MJ/d) between the C and T groups was somewhat larger than intended.
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). The ME requirement for maintenance was calculated as above and an additional allowance of 34 MJ/d was made for pregnancy. In addition to the restricted amount of wilted grass silage, the cows received a mixture of barley and oats. The quantity of cereal mixture was increased from an initial amount of 2 kg/d to 3 kg/d one week before calving. During the final 2 wk of pregnancy, 1 kg/d of molassed sugar beet pulp (G0) or 1 kg/d of glucogenic supplement (G1) was added to the cereal mixture. Average feed intake between d 14 and 1 prepartum is shown in Table 3, and the chemical composition of the feeds given between 3 wk prepartum and 8 wk postpartum is shown in Table 4.
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). The daily concentrate allowance of 15 kg/d was achieved within 16 d after calving. Thereafter, the concentrate allowance remained fixed until the end of the experiment. Until d 4 of lactation, the concentrate was fed 3 times per day (at 0500, 1400, and 2000 h), and thereafter 6 times per day (at 0500, 0800, 1100, 1400, 1700, and 2000 h). All cows were offered wilted grass silage ad libitum (same silage as before calving). The silage was distributed by an automated feeding car 5 times per day (0530 h and 4 times between 1430 and 2000 h).
Sampling, Chemical Analysis, and Measurements
Feed offered and feed refused were recorded daily. The feeds were sampled weekly, and the cereal concentrate and silage samples were pooled to form a monthly sample. Samples of molassed sugar beet pulp, glucogenic supplement, and rapeseed meal were pooled to form a 2-mo sample. Feed samples were analyzed as described by Kokkonen et al. (2000; 2002).
The cows were kept in tie stalls and milked twice daily, and the milk yield was recorded for every milking. The milk samples were taken on 4 consecutive milkings at 1, 2, 4, 6, 8, and 10 wk after parturition. The samples were sent to a commercial laboratory (Valio Ltd., Helsinki, Finland) for analysis of fat, protein, lactose, and urea using infrared procedures (MilkoScan FT6000; Foss Electric, Hillerød, Denmark).
Body weights were recorded on 2 consecutive days 3 wk before the expected calving date, at the day of calving, the following day, and at 1, 2, 4, 6 and 8 wk after calving. To minimize the influence of milking and feeding, the cows were always weighed at the same time of day, before the afternoon feeding. Body condition scoring (5-point scale; Edmonson et al., 1989) was done by the same person throughout the experiment in conjunction with weighing.
Changes in body fat reserves and muscular volume were measured with ultrasonographic scanning. A real-time B-mode ultrasound scanner (Aloka SSD-210DXII, Aloka Co. Ltd., Tokyo, Japan) equipped with a 5.0-MHz linear array transducer for measurements of muscle and a 7.5-MHz transducer for measurements of subcutaneous fat was used. Subcutaneous fat depths (FD) were measured at 3 locations as follows: 1) on the left transversal process of the fourth lumbar vertebra, 2 to 3 cm medially from the lateral end, 2) in the middle of the line connecting the ventral corner of the left tuber coxae and the dorsal tuberosity of the left tuber ischiadicum, and 3) on the same line, 8 cm cranially from the dorsal tuberosity of the tuber ischiadicum. In addition to the subcutaneous tissue, the entire skin layer was included in the measurements. The changes in muscular volume were followed with measurements of the diameter of the longissimus lumborum muscle. The muscle was scanned on the left transversal process of the fourth lumbar vertebra and the largest diameter measured from membrane to membrane. The measurements were performed 5 times: 2 mo before and 7 ± 1 d before the expected calving day, within 24 h after parturition, and 7 ± 1 and 28 ± 2 d after parturition.
Adipose tissue samples were taken at 7 ± 1 d before the expected calving day, within 24 h after parturition,7 ± 1 and 28 ± 2 d after parturition. The biopsy specimen was taken from the subcutaneous fat in the area of the ischiorectal fossa, several centimeters caudally from the sacrotuberous ligament, from the left and right side in turn. Epidural anesthesia was performed with 120 mg of lidocaine hydrochloride (Lidocain 20 mg/mL; Orion Corporation, Espoo, Finland). The region was shaved and washed with soap and disinfectant. A stick incision, about 1 cm in length, was made with a scalpel. Adipose tissue was harvested with a Weil-Blakesley rongeur approximately 20 to 30 times; 2 g of tissue were needed. No further suturing or antibiotic therapy was used.
Adipose tissue fragments were submerged in Krebs-Ringer buffer (Sigma Chemical Co., St. Louis, MO), supplemented with NaHCO3 (Sigma) (15 mmol/L), and with CaCl2 (2.5 mmol/L). The tubes containing buffer and tissue samples were maintained at 37°C and were transported to the laboratory. The tissue fragments were freed as much as possible from the vascular and connective tissue on a glass plate maintained at 37°C with a water bath underneath. The tissue was cut into pieces of 10 to 30 mg, and about 100 mg of tissue were incubated in 3 mL of Krebs-Ringer buffer supplemented with NaHCO3 as described above plus 3% (wt/vol) BSA [Fraction V (fatty acid-free), Roche Diagnostics GmbH, Mannheim, Germany]. Incubation tubes (10 mL) were gassed with O2:CO2 (19:1) and capped. All incubations were carried out in duplicate with shaking (150 oscillations/min) at 37°C. After 15 min, a 1-mL sample of the incubation medium was withdrawn for zero-time analysis. In addition to basal lipolytic rate, the effect of agonist was studied; the agonists used were 50 µmol/L norepinephrine (arterenol, Sigma) and 10 mmol/L glucose (Sigma). After the zero sample and addition of agonists, the tubes were gassed, capped, and incubated for 120 min. The incubations were stopped by placing the tubes on ice for 5 min and a 1-mL sample was withdrawn for analysis. Samples taken from the incubation media were stored at –80°C until analysis. The incubation tubes containing the tissue fragments and approximately 1 mL of incubation media were weighed and placed at 102°C for 24 h to determine the DM content of the tissue sample. The DM content of the incubation media was determined separately and was taken into account in the calculation of tissue DM content.
Lipolysis was monitored by following the release of glycerol, which was assayed with the GPO-Trinder method (McGowan et al., 1983; procedure no. 337; Sigma Diagnostics, Inc., St. Louis, MO) with the following modifications: reagent A was diluted with deionized water (1:1) and the sample and reagent volumes were 10 and 150 µL, respectively.
Blood samples from the mammary vein (vena subcutanea abdominis) were taken before the afternoon feeding at 1300 h (Kokkonen et al., 2000). The preplanned schedule for prepartum sampling was 21, 7, 5, 3, and 1 d before the expected calving date. If calving was delayed, sampling was continued every second day until calving. The samples taken at 21 d before the expected calving date and during the final week before the actual calving were used to determine prepartum blood composition. The interval between blood sampling at 21 d before the expected calving date and the actual calving averaged 23 d (range 13 to 37 d). Due to untimely calving, blood samples from some cows could not be taken in the final week before the calving. In the treatment group CG1, 3 of 4 samples were missing from one cow. In the treatment group TG0, 2 samples were missing from 2 cows. In the treatment group TG1, all 4 samples were missing from one cow, and 1 sample was missing from one cow. After calving, the blood samples were taken at 1, 3, 5, 7, 14, 21, 28, and 56 d postpartum.
ß-Hydroxybutyrate (Hansen and Freier, 1978) was determined from whole blood. Plasma glucose and NEFA were determined with the methods described by Kokkonen et al. (2000). Plasma creatinine was analyzed with the method of Fabiny and Ertigshausen (1971). Plasma 3-methylhistidine (3-MH) concentrations were analyzed with a Biochrom 20 amino acid analyzer (Biochrom Ltd., Cambridge, UK), according to Directive 98/64/EC (European Commission, 1998). Plasma leptin was determined with ovine-specific radioimmunoassay (Delavaud et al., 2000) and validated for bovine plasma (Delavaud et al., 2002). The intra- and interassay CV were 6 and 9%, respectively. Plasma insulin was assayed with commercial radioimmunoassay (Coat-A-Count; Diagnostic Products Corporation, Los Angeles, CA). The intra- and interassay CV for insulin were 8 and 6%.
Calculations and Statistical Methods
Digestibility values taken from feed tables (Tuori et al., 2000) were used for calculating the feeding values of concentrates. The feeding values of silage were calculated using OM digestibility determined in vitro with cellulase solubility (Friedel, 1990). Energy balance was calculated as the difference between ME consumed and ME required for maintenance and milk production. The ME requirement for maintenance was calculated according to MAFF (1975), without the 5% safety margin. Efficiency of ME use for milk production was assumed to be 0.62. A constant value of 3.14 MJ of net energy/kg of energy-corrected milk (ECM) was assumed, and ECM was calculated according to Sjaunja et al. (1991) using the formula: ECM = milk yield (kg) x (38.3 x milk fat (g/kg) + 24.2 x milk protein (g/kg) + 16.54 x milk lactose (g/kg) + 20.7)/3140.
The postpartum data for milk yield and feed intake were reduced to weekly averages and analyzed as repeated measures, using the PROC MIXED procedure of SAS (version 6.12; SAS Institute Inc., Cary, NC). The statistical model included block, time, body fatness, glucogenic supplement, body fatness x glucogenic supplement interaction, body fatness x time interaction, glucogenic supplement x time interaction, body fatness x glucogenic supplement x time interaction, and block x time interaction. For each variable analyzed, a cow nested within the treatment was subjected to 3 covariance structures: compound symmetry (CS), unstructured (UN) and autoregressive order 1 [AR(1)]. The covariance structure that resulted in the largest Schwarz Bayesian criterion was used (Littell et al., 1996).
Milk composition, postpartum ME balance and blood composition data, lipolysis data from norepinephrine stimulation and data on DM content of the adipose tissue biopsy were analyzed as repeated measures with the PROC MIXED procedure as described above, using covariance structures CS, UN, and spatial power law [SP(POW)]. Treatment effects at specific days were determined by use of the DIFF option for the LSMEANS statement. Separate analyses using blood composition data collected during the glucogenic supplementation period were conducted to test the effect of glucogenic supplement and its interactions with body fatness and time.
Some of the lipolysis data (basal rate and effect of glucose) and blood ketone data were not normally distributed; these data were analyzed with Friedman’s 2-way nonparametric ANOVA using SAS. Observations from one cow (in group TG1 at d 28 of lactation) that were more than 3 SD from the mean of the lipolysis data were considered outliers.
Body weight and BCS data and the results of the ultrasound measurements were analyzed with the PROC MIXED procedure with the model including the fixed effect of treatments and random effect of block. Relationships between BCS, FD, EB, and blood hormones and metabolites were calculated using Pearson correlation coefficients in the PROC CORR procedure of SAS.
One cow in the TG1 group suffered from teat injury; the data on this cow were not used for calculation of average milk yield and composition, or calculation of ME balance. The effects were considered to be significantly different at P < 0.05 unless otherwise stated.
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RESULTS AND DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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). Cows in the C groups maintained their BCS during the dry period, whereas the increase in BCS in T group cows was smaller (+0.14) than expected. Theoretically, the additional energy received by the T groups between d 56 and 21 prepartum (38 MJ of ME/d) was sufficient for a BW gain of 1 kg/d. In line with this, BW gain was 1.2 kg/d higher in the T groups than in the C groups between d 56 and 28 prepartum, i.e., a total BW gain of +34 kg (Table 5). This gain would correspond to a BCS gain of 0.8 to 1.0 according to Chilliard et al. (1991). This raises the question of whether the magnitude of the recorded BCS changes in the present study is correct.
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). However, the differences between the T and C groups were not increased during the dry period, which is at variance with the BW gain. Two possible explanations can be offered for this discrepancy. First, increases in internal fat and gut fill may have contributed disproportionately to BW gain. Second, no ultrasound measurements were performed between 8 and 1 wk before calving. Hence, the second measurement was performed 2 wk after the removal of the additional energy allocation from the T groups. Cows in the T groups may have undergone increased lipid mobilization between d 21 and 7 prepartum, which is suggested by a tendency toward higher plasma NEFA concentrations in these cows than in cows in the C groups 7 d prepartum. In support of this, cows in the T groups showed larger decreases in FD between 7 d prepartum and 1 d postpartum than cows in the C groups (–0.9 vs. –0.3 mm, P < 0.05).
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). Milk protein and urea contents were lower (P < 0.05) in the T groups than in the C groups. There was a significant time x body fatness interaction on ECM (P < 0.001).Cows in the T groups tended to increase ECM faster than cows in the C groups during the first 4 wk of lactation.
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). In parallel, steeper decreases in FD were seen in T groups between 1 wk prepartum and 4 wk postpartum (Table 6), and estimated EB was more negative in T groups than in C groups at wk 1 and 2 of lactation (Figure 1).
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In agreement with earlier studies (Kunz et al., 1985; Vazquez-Anon et al., 1994), plasma NEFA was moderately increased during the week preceding calving, peaked at ± 1 d from calving, and began to decrease within 1 wk after calving. Figure 2a shows that the T groups tended to have higher plasma NEFA as calving approached and during the early weeks of lactation. This suggests that, compared with leaner cows in the C groups, the cows in the T groups initiated more extensive mobilization of body fat before calving which continued during the first weeks of lactation. This is in agreement with earlier studies showing higher postpartum BCS or BW losses (Garnsworthy and Topps, 1982; Treacher et al., 1986) or blood NEFA concentrations (Reid et al., 1986; Rukkwamsuk et al., 1998) in overconditioned cows or cows with high-energy prepartum feeding. It must be noted that grass silage was given ad libitum in the present trial and a high daily concentrate allowance (15 kg/d) was achieved rapidly (16 d) after calving. The effect of body fatness at calving on negative energy balance, BW and BCS losses, plasma NEFA increase, and adipose cell size decrease is much more marked when cows are restrictively fed after calving, than in cows fed ad libitum (Chilliard, 1992).
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Blood BHBA and Glucose
The decreased availability of glucose precursors in the liver during early lactation increases ketone body production because of the high rate of gluconeogenesis and limited entry of exogenous nutrients (Chilliard, 1999). Our previous experiment (Kokkonen et al., 2000) showed the antiketogenic potential of glucogenic supplement containing propylene glycol, polyols, and niacin. The current results partly confirm this (Figure 2b). This suggests that cows with larger mobilizable fat depots may benefit from intake of glucogenic supplement. Similarly, a recent review by Nielsen and Ingvartsen (2004) shows that propylene glycol induces the largest decreases in plasma BHBA in animals with higher NEFA concentrations.
Increased BHBA during early lactation of fatter cows in the TG0 group (Figure 2b) is in agreement with the findings of Kunz et al. (1985). Rukkwamsuk et al. (1998) also observed a similar tendency, whereas Reid et al. (1986) and Tesfa et al. (1999) detected no effects of body fatness or dry period overfeeding on blood BHBA. The variation between studies was probably due to differences in milk production levels, feeding regimens, and the dekgree of energy balance and fatty acid mobilization.
The general pattern of plasma glucose concentrations was similar to that seen in previous studies (Kunz et al., 1985; Vazquez-Anon et al., 1994), showing a rapid decrease after calving. The mean glucose concentrations (mg/dL) at d –21, –7, –1, 1, 7, 28, and 56 relative to calving were 68.7, 65.7, 68.8, 67.1, 47.3, 48.8, and 54.7 (pooled SEM = 1.22). The extent of the decrease could be even more dramatic in our study than in earlier studies, due to blood sampling from the mammary vein, and hence increased mammary uptake of glucose during lactation. In accordance with earlier findings (Kunz et al., 1985; Reid et al., 1986; Rukkwamsuk et al., 1998), body fatness had no consistent effect on postpartum glucose concentrations.
Plasma glucose concentrations were not increased with glucogenic supplementation. The increased glucose requirement for lactose synthesis may have accounted for the absence of differences in plasma glucose in the mammary vein between G0 and G1 groups after calving, because the glucogenic supplement tended to increase the milk yield (P = 0.11).
In Vitro Lipolysis
Large differences were observed in lipolytic activity among individual biopsy specimens. Although this made it difficult to detect potential differences between treatments, some clear trends were observed. First, the mean DM content of biopsy specimens decreased from 802 g/kg at calving to 740 g/kg at d 7 postpartum, indicating increased tissue hydration together with increased lipid mobilization; the differences between treatments or treatment x time interaction were not statistically significant. In agreement with our results, earlier studies with lactating goats showed a strong negative correlation of lipid and water contents of adipose tissue (Bas et al., 1987). Second, in contrast to earlier studies (Metz and van den Bergh, 1977; McNamara and Hillers, 1986), the basal rate of glycerol release from adipose tissue samples was decreased at the time of calving (Figure 3a) and did not reach the prepartum level by 28 d postpartum. This discrepancy could be because our cows were fed with a restricted amount of feed during the final weeks of pregnancy. Similarly, Rukkwamsuk et al. (1998) observed a greater decline in basal lipolytic rate with restrictively fed cows than with overfed cows during the periparturient period. Because in vitro glycerol release reflects lipolysis quite well (Chilliard, 1999), this raises the question of whether restricted feeding during the final weeks of pregnancy increases the risk of hepatic lipid accumulation. In the present trial, the plasma NEFA concentration was slightly increased between d 21 (beginning of restricted feeding) and 7 prepartum (Figure 2a). During the final week of pregnancy, plasma NEFA continued to increase; however, the corresponding NEFA profile was also observed with ad libitum feeding (Grummer, 1993). Furthermore, a study by Vazquez-Anon et al. (1994) showed that in the absence of a prolonged DMI depression, liver triglycerides infiltration did not occur until the acute rise in NEFA at calving.
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), which is consistent with the results of Metz and van den Bergh (1977).
The decrease of norepinephrine-stimulated glycerol release at calving (Figure 3b) was not as pronounced as the decrease of basal rate (Figure 3a). In agreement with Rukkwamsuk et al. (1998), norepinephrine-stimulated glycerol release relative to basal rate increased after calving. One week before calving, the norepinephrine-stimulated glycerol release was higher (P < 0.05) in samples taken from cows in the T groups, which received high-energy feeding during the early dry period. The trend (P < 0.10) toward higher response to norepinephrine stimulation could also be seen 1 wk after calving. These results suggest that increased fatness amplifies the lipolytic response of adipose tissue to norepinephrine stimulation, even if the cows are not overfed during the immediate prepartum period.
Protein Mobilization
The longissimus lumborum muscle tended (P = 0.05) to be thicker in T groups 1 wk before calving (Table 6), and at the beginning of the experiment (P = 0.13). Thus, allocating the cows to energy levels according to BCS not only yielded groups with unequal lipid stores but probably also with unequal protein stores in the muscles.
The decrease of muscle diameter started between 7 d prepartum and 1 d postpartum in all groups, suggesting that protein mobilization was initiated before calving. After calving, the decrease of muscle diameter continued until to the last measurement at d 28 of lactation. A parallel decrease of plasma creatinine from 121 to 81 mmol/L between d 1 and 21 of lactation was observed in all groups (Figure 4), indicating a decrease in total muscle mass.
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) between 1 and 28 d postpartum. In line with this, Reid et al. (1986) reported that the muscle (m. trapezius thoracalis) fiber area of fat cows decreased significantly around calving, whereas that of thin cows did not decrease. Thus, cows in the T groups demonstrated more protein mobilization in parallel with more lipid mobilization. The plasma 3-MH measurements were too few to adequately describe protein mobilization postpartum. The mean 3-MH concentrations (µmol/L) at d –7, 1, and 28 relative to calving were 8.8, 13.0, and 5.8 (pooled SEM = 1.28), with no differences between treatments. Nevertheless, at d 28 of lactation, the mean 3-MH concentrations were below the concentrations detected 7 d prepartum, indicating that the most extensive period of protein mobilization was over by that time. This was further supported in the study by Burhans et al. (1997), who found that plasma 3-MH declined to basal levels by 21 d postpartum.
Glucogenic supplement did not decrease amino acid mobilization, as indicated by ultrasound measurements (Table 6) and 3-MH. On the other hand, the decrease of plasma creatinine continued between d 28 and 56 of lactation in G0 groups, whereas plasma creatinine in G1 cows leveled off (Figure 4). This may indicate that protein mobilization was prolonged in G0 groups.
Plasma Leptin
A considerable decrease in plasma leptin during the final days of pregnancy and the first days of lactation (Figure 5a) is in agreement with recent reports (Block et al., 2001; Holtenius et al., 2003; Liefers et al., 2003; Reist et al., 2003) based on ruminant-specific leptin assays. The study by Block et al. (2001) showed that the decrease in leptin is associated with the onset of copious milk production followed by negative EB, because the leptin decrease was not observed in cows that were not milked after parturition. Although the cows in the T groups showed a more negative EB (Figure 1) and more intensive lipid mobilization during early weeks of lactation, they still had higher (P < 0.05) concentrations of plasma leptin than cows in the C groups. Nevertheless, the differences between groups were smaller postpartum than prepartum.
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) were observed between body condition and plasma leptin as well as subcutaneous FD measured with ultrasound and plasma leptin at all days measured, with the slight exception of d 7 after calving. Significant positive correlation between leptin and insulin (and glucose at d –21 and +21) is in agreement with a study by Block et al. (2001), whereas the lack of correlation between leptin and NEFA is not. Blood collection from the mammary vein may account for the absence of correlation. Mammary uptake decreases the concentrations of metabolites during lactation and probably decreases the variability of the concentrations more markedly in mammary than in jugular venous blood.
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) were observed between groups G0 and G1, no obvious rationalization for the tendency toward increased leptin concentration can be given, and we could speculate on an effect of specific nutrients which were present in the supplement or were increased at the gut level during digestion processes. |
CONCLUSIONS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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Fatter cows showed a higher concentration of plasma leptin prepartum and a more pronounced decrease in leptin concentration during the final week of pregnancy and the first week of lactation. Despite a more negative EB, fatter cows still had higher concentration of plasma leptin after calving. Moreover, the glucogenic supplement tended to increase plasma leptin despite the simultaneous tendencies toward increased milk yield and tissue mobilization. These results suggest that plasma leptin concentration in early-lactation cows is primarily and closely associated with body fatness, and could be affected to some extent by specific nutrients.
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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 January 9, 2004. Accepted for publication December 10, 2004.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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