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PubMed1990

The cDNA and protein sequences of mouse lactate dehydrogenase B. Molecular evolution of vertebrate lactate dehydrogenase genes A (muscle), B (heart) and C (testis).

Mouse lactate dehydrogenase-B cDNAs were isolated from cDNA libraries of macrophage (ICR strain) and thymus (F1 hybrid of C57BL/6 and CBA strains), and their nucleotide sequences determined. The lactate dehydrogenase-B cDNA insert of thymus clone mB188 consists of the protein-coding sequence (1002 nucleotides), the 5' (46 nucleotides) and 3' (190 nucleotides) non-coding regions, and poly(A) tail (19 nucleotides), while macrophage clone mB168 contains a partial lactate dehydrogenase cDNA insert from codon no. 55 to the poly(A) tail. Seven silent nucleotide substitutions at codon no. 142, 143, 186, 187, 241, 285 and 292, as well as a single nucleotide change in the 3' non-coding region, were found between these different strains of mice. The predicted sequence of 333 amino acids, excluding initiation methionine, was confirmed by sequencing and/or compositional analyses of a total of 103 (31%) amino acids from tryptic peptides of mouse lactate dehydrogenase-B protein. The nucleotide sequence of the mouse coding region for lactate dehydrogenase B shows 86% identity with that of the human isoenzyme, and only eight of the 139 nucleotide differences resulted in amino acid substitutions at residues 10, 13, 14, 17, 52, 132, 236 and 317. The rates of nucleotide substitutions at synonymous and nonsynonymous sites in the mammalian lactate dehydrogenase genes are calculated. The rates of synonymous substitutions for lactate dehydrogenase genes A (muscle) and B (heart) are considerably higher than the average rate computed from human and rodent genes. The rates of nonsynonymous substitutions for lactate dehydrogenase genes A (muscle) and B (heart), particularly the latter, are highly conservative. The rates of synonymous and nonsynonymous substitutions for the lactate dehydrogenase-C gene are about the same as the average rates for mammalian genes. A phylogenetic tree of vertebrate lactate dehydrogenase protein sequences is constructed. In agreement with the previous results, this analysis further indicates that lactate dehydrogenase-C gene branched off earlier than did lactate dehydrogenase-A and lactate dehydrogenase-B genes.

Amino Acid Sequence↗
PubMed1982

Simultaneous measurements of lactate turnover rate and umbilical lactate uptake in the fetal lamb.

Lactic acid represents a major exogenous nutrient for the developing fetal lamb in utero. Our study was undertaken (a) to quantitate the net consumption of lactate by the fetus, (b) to quantitate the net lactate production and metabolism by the placenta, and (c) to compare the net fetal lactate consumption with fetal lactate use, measured simultaneously with radioactive tracers. 14 pregnant sheep were prepared with catheters in the maternal femoral artery and uterine vein and in the fetal aorta and umbilical vein. By simultaneous application of the Fick principle to the uterine and umbilical circulations, placental glucose consumption and placental lactate production were rapid, averaging 39.8 +/- 5.1 and 11.8 +/- 0.7 mg.min-1. Net lactate umbilical uptake averaged 1.95 +/- 0.16 mg-1.kg.min-1. During infusion of L-[14C(U)]lactate, fetal lactate turnover was much more rapid, averaging 6.5 +/- 0.8 mg.kg-1.min-1, and lactate utilization within the anatomic fetus was 5.9 +/- 0.7 mg.kg-1.min-1. During infusion of tracer glucose, endogenous fetal lactate production from glucose and nonglucose substrates averaged 3.0 and 1.5 mg.kg-1.min-1, respectively. The present studies have quantitated under well oxygenated, steady-state conditions, the rapid placental metabolism and production of lactate, the net fetal consumption of lactate, and the rapid endogenous fetal lactate production from glucose and nonglucose substrates.

Animals↗
PubMed1983

Effect of exogenous growth hormone in early and late lactation on lactational performance of dairy cows.

Bovine growth hormone (51.5 IU/day) and placebo injections were administered for 10 days to four Holstein cows in early lactation (wk 12) and again in late lactation (wk 35). Milk productions in the last 5 days of each period were compared. In early lactation, growth hormone increased milk yield by 15%, fat yield by 17%, protein yield by 14%, and lactose yield by 21%. In late lactation the respective increases were 31, 42, 18, and 35%. For responses of early and late lactation to growth hormone on a quantitative basis, increases for milk yield (4.3 versus 3.9 kg/day) and milk energy secretion (3.3 versus 3.4 Mcal/day) were similar. Concurrent with these increased milk yields, ad libitum intakes of a complete mixed diet declined during the period of growth hormone treatment by 3% in early lactation and 16% in late lactation. During the 6 h immediately following injections of growth hormone, blood plasma concentrations of growth hormone were elevated about 400% in early lactation and 700% in late lactation. Concentrations in plasma of free fatty acids were also higher during growth hormone treatment in late lactation but not in early lactation. Treatments did not affect plasma concentrations of glucose, insulin, glucagon, prolactin, tri-iodothyronine, thyroxine, or cortisol in either early or late lactation. Daily administration of growth hormone in early or late lactation resulted in similar and substantial increases of milk yield and efficiency of milk production.

Animals↗
PubMed1994

Expression of insulin-like growth factor-I in cows at different stages of lactation and in late lactation cows treated with somatotropin.

Relative amounts of IGF-I mRNA were measured in livers of Holstein cows at different stages of lactation (6 early, 6 mid, 6 late lactation, 6 dry) and 6 late lactation cows treated with bST for 1 wk. Milk yield was greater for early lactation cows than for mid and late lactation controls. All cows except those in early lactation were in positive energy balance. Serum IGF-I increased as lactation progressed and was greatest during the dry period. Liver IGF-I mRNA was less in cows in early than in late lactation but greater in lactating than in dry cows. Treatment with bST increased milk yield and concentrations of serum IGF-I, hepatic IGF-I mRNA, and serum IGF-binding protein-3, decreased concentration of serum IGF-binding protein-2, and did not alter abundance of mammary IGF-I mRNA. These parallel changes in serum IGF-I and hepatic IGF-I mRNA suggest that exogenous bST increases IGF-I synthesis in liver of cows during late lactation and that IGF-I synthesis is depressed during early lactation when cows are in negative energy balance. We conclude that IGF-I may play an endocrine role in mediating galactopoietic effects of exogenous bST during late lactation. However, the role of IGF-I during early lactation remains unclear.

Animals↗
PubMed1985

Carrier-mediated uptake of lactate in rat hepatocytes. Effects of pH and possible mechanisms for L-lactate transport.

The rate of uptake and the distribution ratio between intra- and extracellular compartments of L- and D-lactate were studied in hepatocyte preparations from fed rats. L- and D-lactate uptake apparently depended on both passive diffusion and carrier-mediated components. The apparent Km of the high-affinity carrier for L-lactate was in the range of 1.8 mM. The reciprocal competitive inhibitions between isomers of lactate suggest that L- and D-lactate might be transported by distinct carriers. Lactate transport was inhibited by various anions; pyruvate was the most potent anion, whereas only high concentrations of ketone bodies were effective. Acidic extracellular pH enhanced lactate uptake, this effect being more pronounced for L-lactate. At low pH, L-lactate was concentrated into hepatocytes, but its affinity for the carrier appeared unchanged, suggesting the existence of a process gaining energy from the pH gradient across the cell membrane. In the hypothesis of a lactate/H+ symport, the affinity for H+ was not dependent on lactate concentration and the apparent Km for H+ corresponded to a pH of 7.34. No trans-stimulation of lactate uptake after prior loading of the cells with pyruvate or lactate was observed. The present data suggest that, at physiological concentrations, lactate uptake by the liver might be largely carrier-mediated and the rate of transport across the liver cell membrane may be of a magnitude relatively comparable to the rate of metabolism.

Animals↗
PubMed2003

Management factors associated with the incidence of clinical mastitis over the non-lactation period and bulk tank somatic cell count during the subsequent lactation.

AIM: To evaluate associations between management decisions related to the control of mastitis, including the infusion of antibiotics at the end of lactation (dry-cow therapy; DCT), on the incidence of clinical mastitis over the non-lactating period and the bulk tank somatic cell count (BTSCC) in the subsequent lactation. METHODS: Dairy herd owners (n=158) provided information via a retrospective survey about (a) the proportion of their herds treated with DCT; (b) DCT management, including: number of occasions on which cows were dried off; manipulation of feed and water intake around drying off; infusion technique (partial vs full depth insertion of cannula); and hygiene before and after DCT infusion; (c) occurrence of mastitis and frequency of occurrence following drying off and in the subsequent lactation; (d) number of cows culled for mastitis-related conditions; (e) reasons for culling; (f) incidence of clinical mastitis; and (g) stock purchase policy with regard to mastitis. The BTSCC for each vat of milk supplied for the 1999/2000 and 2000/2001 seasons, and records of antibiotic purchases were collated for each herd. The probability that >2% of cows within a herd were diagnosed with clinical mastitis over the dry period was initially examined using univariate analysis (i.e. chi2 or logistic regression) and associated factors (p<0.2) were offered to a reverse stepwise logistic regression model. Factors hypothesised as being associated with the average lactation log10 BTSCC for the 2000/2001 season were initially examined using univariate analysis (i.e. ANOVA or linear regression analysis) and associated factors (p<0.2) were then tested using a forward manual model-building approach. RESULTS: Increasing the percentage of the herd treated with DCT at the end of lactation was associated with reduced probability that >2% of a herd would be diagnosed with clinical mastitis over the non-lactating period and with a lower BTSCC in the subsequent lactation (p<0.01). A lower BTSCC was associated with small herds (<150 cows; p<0.05), not reducing feed intake around drying off (p<0.05), checking for clinical mastitis over the dry period in the milking parlour rather than at pasture (p<0.05), partial insertion of the DCT cannula (p<0.01), and use of 'change in udder shape' during lactation as a diagnostic criterion for mastitis (p<0.05). The incidence of clinical mastitis over the dry period was positively associated with reduced feeding around drying off (p=0.05) and the estimated volume of milk being produced at the time of drying off (p=0.014). CONCLUSIONS: Use of dry cow therapy was associated with fewer cases of clinical mastitis over the non-lactating period and reduced BTSCC over the subsequent lactation. Reduced BTSCC was also associated with smaller herds, use of partial (compared with full depth) insertion of the DCT cannula, not reducing feed intake at the time of drying off, checking for clinical mastitis over the dry (non-lactation) period in the milking parlour, and use of udder shape for diagnosis during lactation. Control of clinical mastitis and BTSCC involves a range of management practices that need to be used in conjunction with DCT. KEYWORDS: Dairy cows, mastitis, dry-cow therapy, somatic cell count, management practices.

Journal Article↗
PubMed1975

Relationship of lactate dehydrogenase specificity and growth rate to lactate metabolism by Selenomonas ruminantium.

A lactate-fermenting strain of Selenomonas ruminantium (HD4) and a lactatenonfermenting strain (GA192) were examined with respect to the stereoisomers of lactate formed during glucose fermentation, the stereoisomers of lactate fermented by HD4, and the characteristics of the lactate dehydrogenases of the strains. GA192 formed L-lactate and HD4 formed L-lactate and small amounts of D-lactate from glucose. HD4 fermended L- but not D-lactate. Both strains contain nicotinamide adenine dinucleotide (NAD)-specific lactate dehydrogenases, and no NAD-independent lactate oxidation was detected. Continuous cultures of both strains grown with limiting glucose produced mainly propionate and acetate and little lactate at dilution rates less than 0.4/h, with shifts to increasing amounts of lactate and less acetate and propionate as the dilution rate was increased from 0.4/h to approximately 1/h.

Acetates↗
PubMed1981

L-Lactate and D-Lactate carriers on the fetal and the maternal side of the trophoblast in the isolated guinea pig placenta.

The transfer of 14C-labelled D- or L-lactate (test substance) relative to 3H-L-glucose (control substance, extracellular marker) into the trophoblast of the isolated guinea pig placenta was determined during an open loop perfusion on both sides. Using a single passage, paired tracer dilution technique, the maximal lactate uptake (Umax) was derived from the venous concentration ratio of lactate to L-glucose. A significant metabolism of L-lactate was not observed. The lactate uptake, which occurred in all placentas studied, was not significantly different on the fetal and maternal side. Within one placenta the L-lactate uptake was always higher than the D-lactate uptake. The uptake of both L- and D-lactate could be inhibited by phloretin. The lactate uptake was inversely correlated with the pH of the perfusate fluid within the range from 6.2-8. A first order saturation kinetic (Hofstee-plot) was used to approximate the relationship between the L-lactate uptake and the chemical L-lactate concentration. We conclude that similar lactate carriers exist in the membranes on both the maternal and the fetal side of the trophoblast.

Animals↗
PubMed1979

Differences between lactating and non-lactating dairy cows in concentration and secretion rate of insulin.

1. Four parameters of insulin metabolism were compared in catheterized lactating and non-lactating Friesian x Ayrshire dairy cows. 2. The four parameters, i.e. arterial and portal-venous concentrations of insulin, and pancreatic output and hepatic uptake of insulin, were approx. 2-, 3-, 3- and 5-fold higher respectively in the non-lactating cows than in the lactating cows in the normal fed state. Statistical significance was not achieved for the differences in magnitude in the case of the latter two parameters, however. 3. All four parameters increased significantly about 4-fold when non-lactating cows were infused intravenously with glucose for 48 h at a rate of 4.2 mmol/min. The parameters also increased in the lactating cows during glucose infusion, but the values reached were substantially lower than in the non-lactating cows and the increases were not statistically significant. 4. Arterial insulin concentrations doubled in the non-lactating cows during a 3 h infusion of propionate into a mesenteric vein, but remained unaltered in the lactating cows. 5. Differences in insulin concentration and output between the lactating and non-lactating cows were not consistently related to differences in either glucose concentration or glucose-entry rate. Arterial propionate concentrations were similar in both groups of cows at all times. 6. It is concluded that in the dairy cow, insulin secretion in response to an insulinotropic agent is diminished during lactation.

Animals↗
PubMed2005

Comparison of the Lactate Pro and Analox GM7 blood lactate analysers.

The purpose of this study was firstly, to determine the level of agreement between the Lactate Pro and Analox GM7 for the measurement of blood lactate, and secondly, to examine whether these analysers may be used interchangeably to identify lactate parameters routinely used in the physiological assessment of athletes. Twenty well-trained male cyclists performed an incremental cycle ergometry test; duplicate blood samples were taken simultaneously throughout the test for lactate determination using the two analysers. Power output and heart rate at LT, LT1, 2 mmol.L-1, and 4 mmol.L-1 were calculated from the lactate values obtained from the two analysers. There was a strong linear relationship between the two analysers (Lactate Pro=1.4541xAnalox GM7-0.1287; R2=0.969, p<0.001; SEE=0.704) though the Lactate Pro overestimated blood lactate when compared to the Analox GM7; 95% ratio limits of agreement (Lactate Pro/Analox GM7) were 1.40x//1.35. Differences were found between analysers for power output and heart rate at LT1 (p<0.01), 2 mmol.L-1 (p<0.001), and 4 mmol.L-1 (p<0.001); no differences were found between analysers for power output or heart rate at LT. In conclusion, the average difference in blood lactate concentration measured by the Lactate Pro and the Analox GM7 was 40%, with 95% of measures differing by between 4% and 89%. This poor level of agreement and the significant differences between the two analysers in power output and heart rate associated with a number of lactate parameters indicate that these analysers should not be used interchangeably.

Adult↗
PubMed1989

Rates of lactate appearance and disappearance and brain lactate balance after oral glucose in the dog.

After glucose ingestion, arterial lactate concentrations increase. Although it is presumed that this is due to an increase in lactate production, rates of lactate appearance have not been measured after oral glucose nor has the major site of its production been identified. Since brain takes up a substantial portion of an oral glucose load but does not store appreciable amounts of glucose, it is possible that brain could be an important site for postprandial lactate formation. Therefore, to investigate the contribution of the brain to the increase in arterial lactate after glucose ingestion and to determine whether changes in lactate appearance or disappearance were predominantly involved, we measured lactate fluxes and brain lactate balance in dogs after intraduodenal administration of glucose (1.6 g/kg). Although systemic lactate appearance increased significantly after glucose administration (from 22 +/- 3 to 33 +/- 9 umole/kg/min, P less than 0.05), brain lactate output did not change (0.62 +/- 0.5 vs 0.74 +/- 0.5 umole/min). We conclude that after glucose ingestion, arterial lactate increases as a result of an increase in the rate of lactate appearance and that brain does not make a significant contribution to this.

Administration, Oral↗
PubMed1994

Maternal protein reserves and their influence on lactational performance in rats. 2. Effects of dietary protein restriction during gestation and lactation on tissue protein metabolism and Na+, K(+)-ATPase (EC 3.6.1.3) activity.

Changes in tissue protein synthesis and an associated membrane transport system in rats were investigated during lactation and under conditions of dietary protein restriction. Following mating, female Sprague-Dawley rats (second parity) were caged individually and offered a high-protein diet (H; 215 g crude protein (N x 6.25; CP)/kg dry matter (DM)) ad lib. until day 12 of gestation. Subsequently half continued to receive diet H, whilst the remainder were offered a low-protein diet (L; 65 g CP/kg DM) until parturition. On day 1 of lactation females were then allocated to either diet H or another low-protein diet (L2; 90 g CP/kg DM) which were offered ad lib. until day 13 of lactation, giving four lactation groups HH, LH, HL2 and LL2. On days 1 and 13 of lactation groups of females were used in the estimation of tissue protein synthesis (flooding dose of [3H] phenylalanine) and Na+, K(+)-ATPase (EC 3.6.1.3) activity (polarographically) in skeletal muscle, mammary gland, liver and duodenal mucosa. By day 1 of lactation diet L had reduced fractional and absolute synthesis rates (FSR and ASR) of muscle protein (P < 0.05) and the O2 consumption associated with Na+, K(+)-ATPase, although not significantly (P < 0.10). Rates of protein synthesis in the other tissues studied were not affected on day 1 of lactation by the gestation dietary treatment. By day 13 of lactation the feeding of diet L2 had reduced muscle FSR and ASR of group HL2 to rates that were lower than those on day 1 (P < 0.05), comparable to those of group LL2 and lower than those of groups HH and LH (P < 0.05). Diet H had allowed group LH to increase their muscle protein synthesis compared with that on day 1 (P < 0.05). Muscle Na+, K(+)-ATPase activity on day 13 of lactation was also lower in groups offered diet L2 (P < 0.05). Mammary protein synthesis was increased during lactation with the feeding of diet H (P < 0.05), which was prevented by diet L2 such that rates of groups HL2 and LL2 were lower than those of the two high-protein groups on day 13 (P < 0.01). Mammary respiration and in particular Na+, K(+)-ATPase activity was increased during lactation by the feeding of diet H (P < 0.05). Rates of protein synthesis and respiration in liver and duodenal mucosa were not significantly affected by the gestational or lactational dietary treatments.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

L-(+)-lactate infusion into working dog gastrocnemius: no evidence lactate per se mediates VO2 slow component.

Constant-load exercise that engenders a sustained lactic acidosis (i.e., above the lactate threshold) is accompanied by a slow component of O2 uptake (VO2) kinetics that increases VO2 above rather than toward the predicted value. This response arises predominantly from within the exercising limbs and is temporally correlated with that of blood lactate. Lactate exerts a disproportionate metabolic stimulatory effect on gluconeogenic tissues, and there is a strong indication that lactate infusions may increase VO2 of resting tissues. To investigate the potential role of lactate in the VO2 slow component, we infused lactate in 20-min square-wave pulses (change of 10 mM) into the arterial blood supply of an electrically stimulated and surgically isolated dog gastrocnemius preparation (2 x 60-min bouts, approximately 30-40% peak VO2; n = 5) under iso-pH conditions at constant muscle temperature. With lactate infusions, intramuscular lactate concentration ([La]) rose proportionally with inflowing [La] (muscle [La] = 6.34 + 0.38 blood [La]; r = 0.642, P < 0.05) to approximately 80% of arterial blood [La], and neither blood (control, 7.39 +/- 0.01; high lactate, 7.40 +/- 0.01; P > 0.05) nor muscle (control, 7.02 +/- 0.03; high lactate, 7.00 +/- 0.04; P > 0.05) pH was changed. Compared with control values, lactate infusion decreased muscle VO2 from 5.1 +/- 0.3 to 4.1 +/- 0.2 ml.min-1.100 g-1 (P < 0.05). However, VO2 relative to tension remained constant. Notwithstanding the obvious differences between this preparation and the exercising human, this finding does not support a role for lactate per se in driving the VO2 slow component during intense exercise.

Animals↗
PubMed1990

Metabolic responses to euglycaemic hyperinsulinaemia in lactating and non-lactating sheep in vivo.

Glucose utilization and production and changes in concentrations of plasma metabolites were studied in lactating and non-lactating sheep in response to three levels of insulin infusion whilst maintaining euglycaemia. Glucose utilization and production responded to insulin infusion similarly in both lactating and non-lactating ewes but, as circulating concentrations of insulin were lower in lactating animals, these parameters appeared more sensitive to plasma concentrations of insulin in lactating sheep. Changes in plasma concentrations of glycerol and free fatty acids during lactation indicated reduced sensitivity to insulin in adipose tissue and changes in plasma concentrations of amino acids were also less during lactation, suggesting reduced sensitivity of protein synthesis to insulin. Changes in plasma concentrations of urea and beta-hydroxybutyrate during lactation were similar to those in non-lactating animals, indicating similar insulin sensitivity of hepatic metabolism. It is concluded that during lactation ovine adipose tissue and muscle are more resistant to increased concentrations of insulin but that the sensitivity of the sheep liver is unchanged or increased. The rate of removal of insulin from the circulation was higher in lactating animals.

Animals↗
PubMed1999

Effect of protein intake during gestation and lactation on the lactational performance of primiparous sows.

The effect of protein intake during gestation and lactation on the lactational performance of primiparous sows was evaluated using 35 Yorkshire x Landrace gilts, allocated to six dietary treatments in a 3 x 2 factorial arrangement. Treatments consisted of three protein levels during gestation, providing approximately 4, 8, and 16 g of lysine/d, and two protein levels (low [L] and high [HI), providing approximately 15 and 45 g of lysine/d, during lactation, respectively. Diets provided similar amounts of ME and all other nutrients. As dietary protein increased during gestation, sows gained more weight and tended to decrease their backfat thickness. There was no gestation x lactation treatment interaction for lactational performance of sows. Feed intake by sows during lactation was usually low but increased (P < .05) with increasing gestation and lactation protein intake and increased linearly (P < .001) as lactation progressed. This linear increase over time was greater (P < .05) in sows fed the H than in sows fed the L protein level. Increased protein intake during lactation reduced (P < .001) 21-d sow weight loss. Milk yield and pig weight gain increased as protein intake increased during gestation (P < .05) and lactation (P < .01). Milk yield did not increase as lactation progressed (P > .05). Pig weight gain increased (P < .05) from wk 1 to 2 of lactation and decreased thereafter. Simple linear regression analysis detected few important relationships between yield of milk components and metabolites or metabolic hormone concentrations. The R2 values for these relationships were < or = .30, except for some relationships between milk component yields and blood urea nitrogen (the range was between .17 and .55). Covariate adjustment for metabolite and metabolic hormone concentrations did not eliminate treatment effects in most cases. This suggests that effects of increased protein intake on milk yield are not fully mediated through metabolite and metabolic hormone concentrations.

Amino Acids↗