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Centre for Dairy Research, Department of Agriculture, The University of Reading, Earley Gate, RG6 6AT England
Corresponding author:
C. K. Reynolds; e-mail:
Reynolds.345{at}osu.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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Abbreviation key: ELAC = early lactation, LCFA = long-chain fatty acids, ME = metabolizable energy, MLAC = midlactation, PCV = packed-cell volume, PDV = portal-drained viscera, RQ = respiratory quotient, TSP = total splanchnic
Key Words: long-chain fatty acids • portal-drained viscera • liver • metabolism
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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Blood Sampling Protocol
Benson and Reynolds (2001) described details of the blood sampling protocol and measurement of blood flow. Briefly, 25 sets of blood samples were obtained simultaneously from the mesenteric artery, hepatic portal vein, and hepatic vein on d 7 of water and subsequent oil infusions during an 8-h period (0630 to 1430 h) that included feeding at 0830 h. Continuous mesenteric vein infusion of 
-aminohippurate for measurement of blood flow began 1 h before blood sampling. Blood for nutrient analysis was collected in syringes treated with potassium EDTA (1.6 mg/ml blood), whereas blood for gas analysis was collected in syringes treated with heparin (125 U/ml of blood). Aliquots of blood were immediately frozen in liquid nitrogen for later analysis of ammonia, urea, and individual VFA concentration. Remaining blood was centrifuged at 3000 rpm and 4°C for 20 min and aliquots of plasma immediately frozen in liquid nitrogen for later analysis of L-lactate, BHBA, and NEFA concentration. Tubes containing blood and plasma were immersed in ice until analyzed or frozen as soon as possible. While 25 sample sets were obtained, for analyses other than -aminohippurate and glucose samples were pooled across contiguous sampling times to reduce analytical requirements. This pooling reduced the total number of samples analyzed for each sampling site within a cow-sampling period to 17 for ammonia, urea, BHBA, NEFA, and L-lactate; 11 for blood gases; and 8 for VFA.
Sample Analysis
Measurements of blood packed-cell volume (PCV), hemoglobin, partial pressure of oxygen (O2) and carbon dioxide (CO2), and pH were obtained as soon as possible after the samples were collected using a blood gas analyzer (Instrumentation Laboratories 1302, Warrington, Cheshire, UK). Hemoglobin concentration of blood samples was measured using a commercial kit (Boehringer Mannheim, Lewes, UK), and blood PCV was determined by microcentrifugation. Plasma glucose and -aminohippurate concentrations were measured as soon as possible on a Cobas Mira analyzer (Roche Diagnostic Products, Welwyn Garden City, UK) using enzymatic (Glucose Trinder Assay; Sigma-Aldrich Ltd., Poole, UK) and colorimetric assays (Benson and Reynolds, 2001), respectively. Blood samples for analysis of ammonia and urea content were thawed and diluted with 0.9 part (vol/vol) ice-cold water and 0.1 part (vol/vol) ice-cold 6 M perchloric acid. Supernatants obtained following centrifugation at 10,000 x g for 40 min at 4°C were neutralized with 2 M potassium bicarbonate and centrifuged for 20 min at 1,800 x g and 4°C. The resulting supernatants were analyzed for ammonia concentration using an enzymatic assay (Kun and Kearney, 1974) or frozen (–20°C) for later analysis of urea concentration using a manual version of an automated colorimetric assay described by Reynolds et al. (1988b).
Concentrations of VFA were measured by capillary GLC using a 30-m x 0.25-mm Stabilwax-DA column (Thames Restek, Slough, UK). Blood samples for VFA analysis were prepared as described (Reynolds et al., 1986), except that the anion exchange resin was changed from the BioRex 5 resin (BioRad, Hemel Hempstead, UK) used in the original procedure to AG4X4. The manufacturer changed the BioRex 5 resin after the original procedure for sample cleanup was validated (Reynolds et al., 1986). Using the AG4X4 resin, the recoveries of VFA added to blood during deproteinization, and adjusted for recovery of added internal standard, averaged 99, 99, 99, 98, 100, and 96% for acetate, propionate, n-butyrate, i-butyrate, n-valerate, and i-valerate, respectively. L-Lactate (Gutman and Wahlfeld, 1974), BHBA (Reynolds et al., 1988a), and NEFA (Reynolds et al., 1988a) concentrations of thawed plasma samples were measured using enzymatic methods adapted for use on the Cobas Mira.
Calculations and Statistical Analysis
Plasma flow for the PDV and liver was calculated from -aminohippurate dilution as described previously (Reynolds et al., 1988b), and blood flow was calculated from plasma flow and PCV. Concentrations of O2 and CO2 in blood were calculated using measured partial pressures of O2 and hemoglobin concentrations or partial pressure of CO2 and pH, respectively (Oddy et al., 1984). Net flux of nutrients and gases across the PDV, liver, and TSP tissues was calculated as the product of venous-arterial concentration difference multiplied by plasma flow (Reynolds et al., 1988b). The fluxes calculated are net values, often the result of both metabolite release into and uptake from blood. Using venous-arterial differences, a negative flux represents a net removal from blood and a positive flux represents a net production or release.
The effects of cow, abomasal infusion (water or oil), stage of lactation (ELAC or MLAC), and the interaction between infusion and stage were tested using residual variance with the GLM procedure of SAS (1999). Only 23 of 24 sets of blood samples were obtained due to the loss of one cow’s carotid artery catheter immediately before blood sampling for oil infusion in ELAC. Least squares means reported were all obtained using the full statistical model for ANOVA, and any standard error of the means presented is for n = 6. Due to the small number of cows used (n = 6), differences were considered significant at P < 0.10.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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) were significantly increased by oil infusion (P < 0.02) and were greater in ELAC than MLAC (P < 0.03). There was no effect of oil infusion or stage of lactation on hepatic artery blood flow. Mean PCV for the three blood vessels sampled (Table 1) was decreased in response to oil infusion (P < 0.03) and was greater in MLAC than ELAC (P < 0.01). Both arterial (P < 0.02) and mean (P < 0.05) hemoglobin concentration (Table 1) were decreased by oil infusion.
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) was decreased by oil infusion, whereas in MLAC oil infusion increased arterial concentration of total VFA (lactation stage by infusion interaction [P < 0.09]). This response was largely due to changes in arterial acetate concentration (Table 2), which accounted for 95% of total VFA concentration in arterial blood and had a similar lactation stage by infusion interaction (P < 0.04). Arterial propionate concentration was greater in MLAC than in ELAC (P < 0.01) and was decreased by oil infusion (P < 0.01). Arterial n-butyrate concentration also showed a stage of lactation x infusion interaction (P < 0.03), but the response was inverse to that of acetate; it was increased by oil infusion in ELAC but decreased by oil infusion in MLAC (Table 2). Arterial concentration of i-butyrate, i-valerate, and n-valerate were much lower than the three major VFA, but arterial concentration of i-butyrate (P < 0.07) and i-valerate (P < 0.01) were greater in ELAC than in MLAC and were not affected by oil infusion (P > 0.25). In contrast, arterial n-valerate concentration was greater in MLAC than ELAC (P < 0.02) and increased by oil infusion (P < 0.01 [Table 2]).
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), but in ELAC, net PDV release of n-butyrate (P < 0.01), i-butyrate (P < 0.01), i-valerate (P < 0.02), and n-valerate (P < 0.07) were all greater than in MLAC. Net release of acetate and net removal of n-butyrate, i-butyrate, i-valerate, and n-valerate by the liver were also greater in ELAC than in MLAC (P < 0.10 [Table 2]). There was a net TSP release for all VFA except n-valerate, for which there was a slight net uptake, but net release of acetate accounted for 97% of the net TSP release of total VFA. Net TSP removal of n-valerate was greater in MLAC than in ELAC (P < 0.10), whereas net TSP release of n-butyrate was greater in ELAC than MLAC (P < 0.01).
Net PDV release of i-butyrate and i-valerate and their net removal by the liver were increased in response to oil infusion (P < 0.01 [Table 2]). There also were stage of lactation x infusion interactions for net acetate flux across both PDV and TSP tissues (P < 0.10). For both tissue beds, net acetate flux was decreased by oil infusion in ELAC and increased by oil infusion in MLAC (Table 3). In contrast, net TSP release of i-butyrate (P < 0.08) and i-valerate (P < 0.06) was increased by oil infusion in ELAC and decreased by oil infusion in MLAC.
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]). On a net basis, PDV urea removal averaged 33% of urea released by the liver, whereas ammonia N removal by the liver accounted for 70% of liver release of urea. There was no effect of stage of lactation on net PDV, liver, or TSP flux of ammonia or urea (P > 0.28 [Table 3]). Infusion of oil increased net PDV release (P < 0.01) and liver uptake (P < 0.02) of ammonia, while net TSP flux was unchanged (P > 0.92). Numerical increases in net liver release of urea (Table 3) accounted for 69% of the increase in ammonia nitrogen removal by the liver when oil was infused.
Blood Gases
Arterial blood O2 concentration was decreased (P < 0.03) by oil infusion but was unaffected by stage of lactation (P > 0.53 [Table 3]). Infusion of oil had no effect on net PDV, liver, or TSP removal of O2 (P > 0.65 [Table 3]). Oxygen removal by the TSP was greater in ELAC than MLAC (P < 0.08) due to an increase in liver removal (P < 0.05), as PDV uptake did not differ (P > 0.38). Arterial CO2 concentrations were unaffected by oil infusion (P > 0.81) and stage of lactation (P > 0.75 [Table 3]). Similarly, net flux of CO2 across PDV, liver, and TSP tissues and respiratory quotient (RQ [net CO2 release/net O2 removal]) for the PDV and liver were not affected by stage of lactation or infusion (P > 0.14 [Table 3]).
Plasma Metabolites
Arterial glucose concentration (P < 0.01) and net liver and TSP glucose release were decreased by the oil infusion (P < 0.06 [Table 4]). Arterial glucose concentration was greater in MLAC than ELAC (P < 0.01), but both liver and TSP glucose production were greater in ELAC (P < 0.01). The slight net removal of glucose by the PDV tissues was unaffected by oil infusion (P > 0.6) or stage of lactation (P > 0.2).
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) and, as there was no effect of stage of lactation on net PDV release of L-lactate (P > 0.64), net TSP release of L-lactate was lower in ELAC than in MLAC (P < 0.01 [Table 4]). There were no effects of either stage of lactation or oil infusion on arterial concentration (P > 0.13) or net PDV, liver, or TSP flux of BHBA (P > 0.40 [Table 4]).
Arterial NEFA concentrations were increased by oil infusion (P < 0.02) and were greater in ELAC than in MLAC (P < 0.01 [Table 4]). Greater arterial concentrations of NEFA during oil infusion were associated with increased net uptake of NEFA by liver (P < 0.02). Overall there was a net TSP uptake of NEFA that was increased by oil infusion (P < 0.02). Net PDV release and liver removal of NEFA were greater in ELAC than in MLAC (P < 0.02), such that net TSP removal of NEFA was not affected by lactation stage (P > 0.99).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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The effect of oil infusion on liver plasma flow in the present study was attributed to metabolizable energy (ME) intake during the blood sampling period or to neural or hormonal responses to postruminal oil infusion (Benson and Reynolds, 2001). While oil infusion decreased daily DMI in our study, the reduction occurred late in the day and before the morning milking, and thus feed DMI during the period of sampling was not affected (Benson et al., 2001). In addition, decreases in blood PCV and hemoglobin and arterial O2 concentration also may have contributed to the increase in blood flow during oil infusion. Assuming a constant O2 extraction efficiency, splanchnic blood flow may have increased during oil infusion to compensate for decreased blood O2 level and restore O2 supply. However, this theory is not supported by work elsewhere. Experimentally induced anemia in pregnant sheep had no effect on blood flow to tissues comprising the TSP (Edelstone et al., 1987), or PDV blood flow and O2 removal in preruminant lambs, where PDV O2 extraction efficiency varied inversely with PCV and O2 supply (Holzman et al., 1985). In humans, increased splanchnic blood flow following ingestion of oil was accompanied by an increase in blood PCV, suggesting other factors are responsible for the increased flow observed (Brundin, 1998). In this regard, increased absorption of oleic acid increases blood flow to the mucosa and muscularis of the jejunum of dogs via signals independent of changes in intestinal metabolism (Chou et al., 1985). These authors theorized that oleate effects on intestinal blood flow might facilitate increased lymph flow, aiding any oleate absorption into mesenteric veins. In the present study, increased liver blood flow during oil infusion was due totally to increased portal vein flow and not accompanied by changes in PDV O2 removal, implying a specific effect on PDV blood flow.
The RQ for the PDV (0.39) was low compared to other studies in lactating cows. A mean value of 0.56 (0.71 to 0.43) was reported for the PDV of lactating cows (Reynolds et al., 1988a), and a value of 2.3 was calculated from the data of Baird et al. (1975). The variability of these values may be due in part to the variability of sampling and measurement technique, as well as variations in gut lumen and blood CO2 exchange. The net release of CO2 by the PDV tissues can be attributable to a number of sources, including gut fermentation, respiratory metabolism in gut tissues, and bicarbonate in saliva. In addition, it is required for absorption of VFA and can be transferred directly from arterial blood to the lumen of the gut (Reynolds et al., 1988a). For these reasons, "conclusions concerning the metabolism by tissue cannot be made" from net PDV flux of CO2 (Pell et al., 1986).
The liver, like the PDV, is highly metabolically active and in the present study consumed amounts of O2 similar to the PDV. The RQ for the liver was also low (0.64) compared with previous studies (0.72 for Reynolds et al., 1988a; 0.90 for Baird et al., 1975) in lactating cows. Liver release of CO2 underestimates total production to the extent that CO2 is used for metabolic processes, such as urea synthesis from ammonia (Stryer, 1981). Neither O2 consumption nor net CO2 release by the liver or TSP tissues was affected by oil infusion. Brundin (1998) also noted no difference in TSP O2 consumption after oral or intravenous administration of vegetable oil in humans, despite an increase in blood flow.
Removal of O2 by the PDV was not affected by stage of lactation, but the liver removed more O2 in ELAC. This in part reflects increased liver glucose synthesis, NEFA removal, and perhaps oxidation. This increase in liver O2 use may also explain the increase in liver blood flow observed in early lactation. Although blood flow to the PDV and liver is highly correlated with DMI, liver blood flow was elevated in ELAC despite similar DMI compared with MLAC. This implies that the increase in liver blood flow in ELAC was a result of the metabolic activity and O2 requirement when milk yield and metabolic demands on the liver were increased.
Effects of LCFA Infusion
PDV nutrient metabolism.
Although daily DMI was reduced by oil infusion, net PDV absorption of total VFA was unaffected. As discussed previously, DMI during the 8-h sampling period was unaffected (Benson et al., 2001), and therefore, the supply of fermentable substrates to the rumen, and subsequently total VFA absorption, would be expected to be similar. However, net PDV absorption of branched-chain VFA and ammonia were increased by oil infusion. These results are difficult to explain, as net PDV release of the other VFA was largely unaffected. Possible explanations for increased net PDV absorption of branched-chain VFA and ammonia attributable to oil infusion include an inhibition of gut motility caused by increased intestinal oil supply (Nicholson and Omer, 1983), which may have altered the extent and pattern of fermentation, as well as oxidative metabolism of the gut tissues. Alternatively, hormonal and metabolic effects of oil infusion may have altered the metabolism of PDV tissues, and thereby branched-chain VFA and ammonia release. In addition, inhibitory effects of any unabsorbed oil on hindgut fermentation and microbial growth, and thus ammonia utilization, may have increased net ammonia absorption.
In spite of greater portal vein blood flow during oil infusion, net PDV removal of O2 was unchanged. In addition, oil infusion had no effect on the net PDV release of CO2, BHBA, and L-lactate, which are all products of PDV metabolism of VFA and glucose. These observations suggest that during sampling the metabolic activity of the PDV was dictated more by feed DMI and fermentable energy supply than by total ME and oil infusion, and that increases in blood flow during oil infusion were not a consequence of changes in the metabolic activity of the gut.
Net PDV glucose flux was also not affected by oil infusion and was negative, indicating greater use of arterial glucose than glucose absorption into the portal vein. However, during the course of blood sampling, net PDV glucose flux increased such that there was a shift from net use of glucose to net release approximately 2 h after feeding (Figure 1). This may reflect a postprandial increase in rumen outflow of undigested starch to the small intestine. There was no evidence of a postprandial response of net L-lactate release by the PDV (data not shown), but there was a marked increase in net PDV release of propionate after feeding (Figure 2), suggesting postprandial responses of propionate, but not L-lactate, were dictated by rumen fermentation. This implies that much of the L-lactate absorbed into the portal vein was a product of glycolysis and not silage intake, fermentation, or propionate metabolism during absorption.
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Liver metabolism.
Grummer and Carroll (1991) proposed that fat supplementation spares glucose from oxidation and that this glucose may be utilized for lactose synthesis and milk production. In the present study, milk production was unaffected by oil infusion despite a decrease in daily DMI (Benson et al., 2001) and liver glucose production; therefore, a larger proportion of liver glucose release was used for milk synthesis. Oil infusion decreased liver glucose output without affecting DMI and liver VFA removal during the 8-h sampling period (Table 2). This suggests that abomasal oil infusion had inhibitory effects on liver glucose production independent of precursor supply during sampling.
Abomasal oil infusion increased the maximum possible contribution of propionate and L-lactate to liver glucose output. This reflects the decrease in liver glucose output and the increase in L-lactate uptake by the liver and suggests a decrease in the contribution of other precursors not measured in the current study (amino acids, glycerol, or pyruvate [Lomax and Baird, 1983]). Alternatively, oil infusion may have caused an increase in the nonglucogenic use of propionate, lactate, or other potential sources of glucose carbon. Increases in insulin and decreases in glucagon could also cause a reduction in liver glucose production (Brockman and Laarveld, 1986), but, in the present study, arterial concentration of insulin was reduced by oil infusion, whereas net liver removal of pancreatic glucagon was increased (Benson and Reynolds, 2001). These changes in pancreatic hormones do not explain the decrease in liver glucose release, but they do provide an explanation for the increase in liver L-lactate removal when oil was infused. L-Lactate is utilized via lactate dehydrogenase and pyruvate carboxylase, and the later enzyme is stimulated by pancreatic glucagon (Brockman and Laarveld, 1986).
In vitro work using hepatocytes from sheep, goats, and calves has shown that under certain conditions specific LCFA (oleate and palmitate) can stimulate gluconeogenesis from propionate (Faulkner and Pollock, 1986; Aiello and Armentano, 1988), without altering the glucogenic use of L-lactate (Aiello and Armentano, 1988). However, in the present study, oil infusion decreased liver glucose release and plasma glucose concentration, perhaps via decreased daily DMI or a decreased glucose requirement, rather than a direct effect of infused LCFA on liver metabolism. Drackley et al. (1992) noted a tendency for plasma glucose concentration to linearly decrease with increasing unsaturation and chain length of abomasally infused LCFA, which they attributed to decreased DMI.
There was a net removal of total VFA and release of acetate by the liver, which was unaffected by oil infusion. Net liver removal of branched-chain VFA was increased by oil infusion, but this accompanied an equivalent increase in their net PDV release, and thus net TSP output was unchanged. As often noted (Reynolds, 1995; Nozière et al., 2000), it appeared that the liver removed VFA (with the exception of acetate) in proportion to their supply from the gut. This is illustrated by the patterns of net PDV absorption and liver removal of propionate across the 8-h sampling period (Figure 2). Postprandial increases in net PDV release of propionate were mirrored by increased net liver removal, and, therefore, little variation in net TSP release was observed.
Net removal of NEFA by the liver was increased by oil infusion, presumably due to increased arterial concentration and supply from the PDV, as NEFA are removed by the liver in proportion to their supply by blood (Emery et al., 1992). BHBA is a product of NEFA and n-butyrate metabolism by the liver, but oil infusion had no effect on BHBA production by the liver. The maximum possible contribution of n-butyrate and NEFA removed by the liver to BHBA released was greater than 100% during oil infusion, perhaps reflecting an increase in-liver utilization of NEFA via oxidation or triglyceride synthesis (Emery et al., 1992). In the present study, an increase in the oxidation of NEFA and other metabolites may have contributed to the depression in daily DMI observed when oil was infused. In nonruminants, increases in liver ATP levels due to LCFA oxidation depress appetite and intake (Scharrer and Langhans, 1986; Friedman, 1998).
Effects of Stage of Lactation
PDV nutrient metabolism.
Lomax and Baird (1983) and Reynolds et al. (1988a) have shown increases in portal vein blood flow and net PDV absorption of VFA and L-lactate in lactating cows compared to nonlactating cows. This is largely the result of increased DMI, as numerous studies have shown linear relationships between DM or ME intake and net PDV release of VFA and other nutrients (Lomax and Baird, 1983; Nozière et al., 2000). However, there has been little research measuring changes in splanchnic metabolism of dairy cows at differing stages of lactation. In the present experiment, DMI and net PDV absorption of total VFA, acetate, propionate, L-lactate, and BHBA were similar in ELAC (8 wk) and MLAC (16 wk). Net PDV absorption of ammonia is highly correlated with N intake (Reynolds, 1995) and was similarly unaffected by stage of lactation in the present study. In contrast, absorption of n-butyrate, branched-chain VFA, and n-valerate were greater in ELAC. Reasons for this specific increase in the PDV absorption of longer-chain VFA are uncertain. The response may be related to longer-term adaptation of the rumen microflora to higher DMI as lactation progressed, effects of water intake associated with higher milk yield in ELAC on rumen fermentation, or changes in gut tissue mass and subsequent metabolism of absorbed VFA.
Net PDV release of NEFA was greater in ELAC compared to MLAC. Reynolds et al. (1988a) reported a decrease in net PDV release of NEFA between wk 4 and 8 of lactation. These differences in net PDV release of NEFA were probably due to an increase in lipolysis of adipose tissue drained by the portal vein associated with greater milk energy yield (Benson et al., 2001) or lower DMI (Reynolds et al., 1988a) in ELAC, and thus reduced tissue energy balance.
Liver metabolism.
Net liver removal of propionate was not affected by stage of lactation, but net liver removal of n-butyrate, branched-chain VFA and n-valerate were greater in ELAC, a consequence of the increase in their net PDV release. Net acetate release by the liver was also greater in ELAC compared with MLAC. This may be attributable to increased NEFA removal and metabolism. However, abomasal oil infusion also increased net liver removal of NEFA but had no effect on net liver release of acetate. In very ELAC, greater liver removal of NEFA would be expected to be associated with more NEFA oxidation and ketone body synthesis, but there was no effect of stage of lactation on net liver release of BHBA in the present study. Net glucose release by the liver was higher in ELAC when milk yield and glucose requirement for milk synthesis were greater (Benson et al., 2001), but arterial glucose concentration was lower, perhaps due to an increased use for milk synthesis. In ELAC, greater glucose release by the liver was associated with more liver removal of L-lactate, and thus a decreased net TSP release. This suggests that the metabolic changes associated with increased milk production in ELAC result in a requirement for additional L-lactate to restore liver carbon balance (Reynolds, 1995). Greater L-lactate removal by the liver in ELAC was associated with increased net liver removal of pancreatic glucagons (Benson and Reynolds, 2001), but in contrast to the response to abomasal oil infusion, increased glucagon removal by the liver in ELAC was associated with greater net glucose release.
Increased liver removal of L-lactate in ELAC may in part reflect an increase in Cori cycling of glucose and lactate between the liver and glycolysis in other tissues, as occurs during starvation (Stryer, 1981). In MLAC, when the cows were in more positive tissue-energy balance (calculated tissue-energy balance increased by 13.2 MJ/d), an increased liver-carbon balance and TSP release of lactate to peripheral tissues may support more body fat synthesis in lactating dairy cows, as occurs with increased intake level in growing ruminants (Prior, 1978). Similarly, differences in liver lactate removal, and thus net TSP lactate release, have been positively associated with increased tissue energy and fat retention in growing cattle (Reynolds et al., 1991; Reynolds, 1995). In the present study, net TSP flux of NEFA was negative, representing liver removal of NEFA from peripheral tissues, and not affected by stage of lactation. However, tissue exchanges of blood NEFA do not account for LCFA exchange via lipoproteins.
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CONCLUSIONS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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ACKNOWLEDGEMENTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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FOOTNOTES |
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2 Current address: Department of Animal Sciences, The Ohio State University, OARDC, 1680 Madison Ave., Wooster 44691-4096.
Received for publication August 17, 2001. Accepted for publication January 11, 2002.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONCONCLUSIONSACKNOWLEDGEMENTSREFERENCES |
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-ketoisocaproate metabolism and interconversions in fed and fasted sheep. Metabolism 35:1005–1016.[Medline]This article has been cited by other articles:
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R. Berthiaume, M. C. Thivierge, R. A. Patton, P. Dubreuil, M. Stevenson, B. W. McBride, and H. Lapierre Effect of Ruminally Protected Methionine on Splanchnic Metabolism of Amino Acids in Lactating Dairy Cows J Dairy Sci, May 1, 2006; 89(5): 1621 - 1634. [Abstract] [Full Text] [PDF]
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G. B. Huntington, D. L. Harmon, and C. J. Richards Sites, rates, and limits of starch digestion and glucose metabolism in growing cattle J Anim Sci, April 1, 2006; 84(13_suppl): E14 - E. [Abstract] [Full Text] [PDF]
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B. J. Bradford and M. S. Allen Phlorizin Administration Increases Hepatic Gluconeogenic Enzyme mRNA Abundance but Not Feed Intake in Late-Lactation Dairy Cows J. Nutr., September 1, 2005; 135(9): 2206 - 2211. [Abstract] [Full Text] [PDF]
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M. D. Hanigan, C. K. Reynolds, D. J. Humphries, B. Lupoli, and J. D. Sutton A Model of Net Amino Acid Absorption and Utilization by the Portal-Drained Viscera of the Lactating Dairy Cow J Dairy Sci, December 1, 2004; 87(12): 4247 - 4268. [Abstract] [Full Text] [PDF]
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M. J. Hersom, C. R. Krehbiel, G. W. Horn, and J. G. Kirkpatrick Effect of the live weight gain of steers during winter grazing on digestibility, acid-base balance, blood flow, and oxygen consumption by splanchnic tissues during adaptation and subsequent feeding of a high-grain diet J Anim Sci, December 1, 2003; 81(12): 3130 - 3140. [Abstract] [Full Text] [PDF]
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J. D. Sutton, M. S. Dhanoa, S. V. Morant, J. France, D. J. Napper, and E. Schuller Rates of Production of Acetate, Propionate, and Butyrate in the Rumen of Lactating Dairy Cows Given Normal and Low-Roughage Diets J Dairy Sci, November 1, 2003; 86(11): 3620 - 3633. [Abstract] [Full Text] [PDF]
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C. K. Reynolds, P. C. Aikman, B. Lupoli, D. J. Humphries, and D. E. Beever Splanchnic Metabolism of Dairy Cows During the Transition From Late Gestation Through Early Lactation J Dairy Sci, April 1, 2003; 86(4): 1201 - 1217. [Abstract] [Full Text] [PDF]
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