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* Laboratory for Animal Nutrition and Animal Product Quality, Faculty of Bioscience Engineering, Ghent University, Proefhoevestraat 10, 9090 Melle, Belgium
Adaptation Physiology Group, Wageningen Institute of Animal Sciences, Wageningen University, PO Box 338, 6700 AH Wageningen, the Netherlands
1 Corresponding author: veerle.fievez{at}UGent.be
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ABSTRACT |
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 TOP ABSTRACT ACKNOWLEDGEMENTSREFERENCES |
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Key Words: dairy cow • subclinical ketosis • milk fatty acid
At the onset of lactation, the dairy cow must accommodate a tremendous increase in energy demand by the mammary gland for milk production. This is realized partly by increasing feed intake and partly by fat mobilization from adipose tissue. However, excessive fat mobilization can induce an imbalance in hepatic carbohydrate and fat metabolism, characterized by elevated concentrations of ketone bodies (BHBA, acetoacetate, and acetone), a state called hyperketonemia (Goff and Horst, 1997; Nielsen and Ingvartsen, 2004). Hyperketonemia has an economical effect in its clinical manifestation (ketosis), through a decreased milk production and greater risk of periparturient diseases such as mastitis (Duffield, 2000). Detection of the preclinical stage of ketosis should allow early intervention, which is beneficial both from an economical and an animal welfare point of view. Current detection methods are based on the measurement of ketone bodies in body fluids, and recent research has been focused toward their detection in milk because of its convenience of sampling (Enjalbert et al., 2001; De Roos et al., 2007). Because mobilization of adipose tissue precedes ketosis development (Reist et al., 2003) and mobilized fatty acids (FA) are incorporated in milk fat, changes in milk FA composition might be an earlier indicator of hyperketonemia.
Data and samples originated from the experiment of Van Knegsel et al. (2007) assessing energy balance from 3 wk before the expected calving date to 9 wk postpartum. The original aim of the experiment was to study strategies to decrease the severity of the negative energy balance at the beginning of lactation. Of 76 cows (both multiparous and primiparous) in the experiment of Van Knegsel et al. (2007), 22 (3 glucogenic, 11 lipogenic, 8 mixed lipogenic:glucogenic; cow diet) showed blood plasma BHBA concentrations beyond the threshold of 1.2 mmol/L in the first 9 wk postpartum. Because the dietary strategy based on a glucogenic concentrate demonstrated lower plasma NEFA, BHBA, and liver triacylglycerol concentrations, this treatment was excluded for the current study. The 2 other dietary strategies did not systematically affect the former parameters.
Cows received forage ad libitum (prepartum: grass silage:corn silage:wheat straw, 450:450:100; postpartum: grass silage:corn silage:chopped alfalfa hay:rapeseed meal, 484:449:33:33; proportions on DM basis) supplied with a lipogenic (n = 25) or a mixed glucogenic:lipogenic concentrate (n = 24) in amounts varying with parity and lactation week. Based on the realized feed intake, starch: 104 and 179 g/kg of DM, crude fat: 50 and 41 g/kg of DM and, net energy: 6.81 and 6.84 MJ/kg of DM [according to the Belgian-Dutch system (VEM) of net energy for lactation; Van Es, 1975] were calculated for the lipogenic and glucogenic:lipogenic diet, respectively.
Body condition was scored (1 to 5 scale) in wk -3, 1, 4, and 8 relative to the week of calving. Energy balance was calculated per week according to the Belgian-Dutch system (VEM) of net energy for lactation system as described by Van Knegsel et al. (2007). Weekly collected jugular blood was analyzed for BHBA and NEFA with the Ranbut and FA 115 kits, respectively (Van Knegsel et al., 2007; Randox Laboratories Ltd., Crumlin, UK), on a Unicel DxC 600 analyzer (Beckman Instruments B.V., Mijdrecht, the Netherlands). Milk production was recorded daily. Milk composition variables (fat, protein, and SCC: ISO 9622, ISO, 1999; Melkcontrolestation, Zupthen, the Netherlands) were monitored 4 times per week. Pooled Wednesday evening and Thursday morning milk samples (50/50, wt/wt) were analyzed for milk FA after extraction, methylation, and GLC as described by Lourenço et al. (2005) and were expressed as grams per 100 g of FA methyl esters (FAME). Proportions of short-chain FA, medium-chain saturated FA (MCSFA), and long-chain FA (LCFA) were calculated as the sum of C4:0, C6:0, and C8:0; C10:0, C12:0, and C14:0; and C18:0, total C18:1, total C18:2, total C18:3, C20:0, and total C20:1 proportions in milk fat, respectively.
To compare the milk FA profile, 2 groups have been created from the data set by selecting cows based on plasma BHBA concentrations (Table 1
). Multiparous cows with plasma BHBA concentration above a threshold value of 1.2 mmol/L (n = 8) in either wk 3, 4, or 5 in lactation, but not showing elevated BHBA concentrations in other weeks, were classified as subclinically ketotic (SCK). The control group consisted of cows (n = 8) showing normal plasma BHBA concentration (<1.2 mmol/L) during the whole registration period and were selected from the data set to approach a similar distribution of milk yield, dietary management, crude fat intake, parity, and SCC, in decreasing order of importance (Table 1).
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Statistical analysis was performed with SPSS 12.0 (SPSS Inc., Chicago, IL) using a nonparametric t-test for group comparison and a 1-way ANOVA for period comparison.
No differences in BCS were measured between groups, and the overall mean BCS scores of both groups were 3.31 ± 0.1, 3.18 ± 0.1, 2.88 ± 0.09, and 2.86 ± 0.09 in wk -3, 1, 4, and 8 relative to calving, respectively. The SCK-diagnosed cows tended to have a more negative energy balance in the prediagnosis period [SCK: -274 ± 47, control: -150 ± 40, kJ/(kg0.75•d); P = 0.099] and had a significantly lower negative energy balance in the diagnosis period compared with control cows [SCK: -138 ± 23, control: -61 ± 36, kJ/(kg0.75•d); P = 0.048].
Milk FA proportions, given in Figure 1, indicate an increase in MCSFA and a decrease in LCFA, particularly C18:1 cis-9 from the prediagnosis to diagnosis and from the diagnosis to postdiagnosis period. This is in line with the effect of lactation stage on milk FA profile reviewed by Palmquist et al. (1993). In none of the 3 registration periods, differences occurred between the 2 groups in milk fat content and milk fat:protein ratios (data not shown).
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Because milk LCFA originate both from fat mobilization and diet, these milk FA can be strongly influenced by the amount of LCFA in the diet. Similar differences in the milk fat C18:1 cis-9 proportions as observed between SCK and control cows have been induced through dietary modification, such as supplementation of linseed, sunflower, and rape oil seeds (4.0, 5.2, and 10.6 units greater in the supplemented groups compared with the nonsupplemented control, g/100 g of total FA; e.g., Chilliard and Ferlay, 2004). In the current study, a similar distribution in dietary management and crude fat intake of the control and SCK group has been attempted (Table 1
). Moreover, palmitic acid, being the major FA in the dietary fat supplement, was omitted from the milk FA analysis. Hence, it is unlikely that changes between the control and SCK group are of dietary origin in this experiment. Milk MCSFA, LCFA, C18:0, and C18:1 cis-9 secretions, estimated as milk fat content multiplied with FAME proportions and corrected for glycerol, did not differ, except for a tendency in greater C18:1 cis-9 secretion in SCK cows compared with control cows in the diagnosis period (0.36 vs. 0.29 kg/d, P = 0.07).
In conclusion, elevated proportions of C18:1 cis-9 are visible in milk fat 2 wk before the SCK diagnosis, making it an interesting trait for SCK prediction. Yet, concentrations deduced from this experiment should only be used within the constraints of the current experiment, because variations of C18:1 cis-9 milk fat proportions are affected by, for example, lactation stage and feed composition. A wider experiment or metaanalysis assessing the relationship between SCK-diagnosed and healthy cows in relationship to lactation stage and dietary fat content could assess the validity of milk C18:1 cis-9 concentrations as a diagnostic tool for predicting SCK.
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ACKNOWLEDGEMENTS |
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TOPABSTRACTACKNOWLEDGEMENTSREFERENCES |
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Received for publication May 19, 2008. Accepted for publication August 18, 2008.
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