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PubMed2001

Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation.

OBJECTIVE: To determine the relative contribution of the gastrointestinal tract and the liver in lactate metabolism in patients with acute liver failure (ALF) and the effect of liver transplantation on this. We hypothesized that the liver and gut are net producers of lactate in ALF and that this is reversed after liver transplantation. SETTING: A university-affiliated specialist liver transplant operating theater. SUBJECTS: Eleven patients with ALF undergoing liver transplantation. MEASUREMENTS AND INTERVENTIONS: After ethical approval, 11 patients with ALF listed for orthotopic hepatic transplantation were studied. Whole blood was analyzed for lactate concentration from radial artery (RA) catheter, portal vein (PV), and hepatic vein (HV) during the dissection phase and was repeated postreperfusion of the liver graft. Gradients across the gut and the liver were calculated to see if there was net production or consumption. RESULTS: HV lactate was significantly higher than arterial (p =.028) in patients with ALF before liver transplantation, suggesting splanchnic production of lactate. Total splanchnic lactate gradient (HV-RA) is positive in ALF. Both the gut (PV-RA) and the liver (HV-PV) were net producers of lactate. After liver transplantation, hepatic venous lactate falls below arterial levels but not significantly. The gradient across the gut (PV-RA) remained positive, but the transhepatic gradient (HV-PV) became significantly negative, showing consumption by the graft (p =.021). The magnitude of lactate consumption after transplantation correlated positively with portal venous lactate concentration (p =.029) and inversely with graft cold ischemic time (p =.007). CONCLUSION: The liver is a net producer of lactate in patients with ALF and an elevated whole blood lactate. After liver transplantation, the graft becomes a consumer of lactate as shown by the negative lactate gradient. The degree of consumption is dependent on portal venous lactate concentration and cold ischemic time.

Female↗
PubMed2007

Lactate down-regulates cellular poly(ADP-ribose) formation in cultured human skin fibroblasts.

BACKGROUND: Polyadenosine diphosphate-ribose (poly(ADP-ribose)) is a nuclear polymer which is derived from nicotinamide adenine dinucleotide (NAD(+)) catalysed by poly(ADP-ribose) polymerase 1 (PARP-1). Aside from the well known role of poly(ADP-ribosyl)ation (pADPR) in DNA repair, pADPR is also involved in other cellular processes such as apoptosis and gene expression. However, the factors that regulate the level of pADPR are not fully elucidated. In view of the fact that healing wounds contain high concentrations of lactate (10-15 mM) and exogenous lactate reduce the NAD(+) pool in cultured fibroblasts, we propose that high lactate lowers the level of nuclear pADPR. MATERIALS AND METHODS: Neonatal human dermal fibroblasts (NHDF) were plated to subconfluence and allowed to adhere. Cells were treated with 15 mM l-lactate and pADPR production was assessed by immunofluorescence analysis using 10H antibody. Difference in pADPR production was determined by calculation of positively stained cells compared to total cell numbers. Inhibition of PARP activity was tested by treatment with 100 microM 3-aminobenzamide (3-AB). Specificity of the lactate effect on pADPR synthesis was verified by using the analogue d-lactate. The contents of nicotinamide adenine dinucleotide (NAD(+)) and its reduced form (NADH) in lactated and non-lactated cell cultures were quantified by the enzymatic cyclic assay. RESULTS: We found that exogenous l-lactate (15 mM) can significantly depress pADPR content in cultured fibroblasts. PARP-1 activity was inhibited by 3-AB and analogue d-lactate showed no effect on pADPR synthesis. NAD(+)/NADH ratio was significantly lowered in lactated compared to non-lactated cell culture. CONCLUSIONS: Exogenous l-lactate (15 mM) can depress pADPR content in cultured fibroblasts. In view of the fact that healing wounds contain such high concentrations of lactate, we propose that down regulation of pADPR is associated with elevated tissue repair via pADPR dependent gene expression. This observation is important in understanding the stimulation of lactate-mediated protein expression during wound healing.

Cells, Cultured↗
PubMed2001

Fetal and maternal lactate increase during active second stage of labour.

OBJECTIVE: To determine longitudinally fetal and maternal blood lactate concentrations during the second stage of labour. DESIGN: Prospective, observational study of randomly selected labours. SETTING: Labour ward, Sultanah Aminah General Hospital, Johore Bahru, Malaysia. MAIN OUTCOME MEASURES: Fetal scalp and maternal venous blood lactate, umbilical arterial and vein lactate and acid-base balance at delivery. RESULTS: Sixty-nine women and their infants were monitored in the second stage of labour. Mean maternal venous lactate by the end of the first stage was 2.6 +/- 1.0 (+/- S.D.) mmol/L and increased to 3.6 +/- 1.4, 4.2 +/- 1.7. 4.8 +/- 1.6, 5.4 +/- 2.1 and 4.3 +/- 0.9 mmol/L, respectively, for every 15 minute of bearing down. Corresponding values for fetal scalp blood lactate were 2.4 +/- 1.1, 3.1 +/- 1.6, 3.2 +/- 1.8, 4.2 +/- 2.4, 4.9 +/- 2.8 and 5.8 +/- 1.9 mmol/L. The mean slope of maternal lactate increase was 0.070 mmol/L per minute (95% CI 0.050, 0.090) and for fetal lactate increase 0.032 mmol/L per minute (95% C.I.: 0.018, 0.045). The duration of active second stage was significantly associated with fetal lactate (P < 0.001) and maternal lactate (P = 0.03) at the time of crowning of the fetal head, and lactate in umbilical arterial and vein blood at delivery (P < 0.001). Expulsion time > or = 45 minutes, compared with shorter active second stage, and acidaemia at birth implied larger arterial-venous lactate differences (P < 0.001). Fetal lactate at crowning was also significantly associated with the umbilical arterial-veonus lactate difference (P = 0.03). CONCLUSIONS: Maternal and fetal lactate concentrations increase significantly with duration of the active second stage of labour, more rapidly in the mother. It is likely that fetal anaerobic metabolism is the main source for the fetal lactate increase.

Adult↗
PubMed2004

Lactate metabolism: a new paradigm for the third millennium.

For much of the 20th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage. Since the 1970s, a 'lactate revolution' has occurred. At present, we are in the midst of a lactate shuttle era; the lactate paradigm has shifted. It now appears that increased lactate production and concentration as a result of anoxia or dysoxia are often the exception rather than the rule. Lactic acidosis is being re-evaluated as a factor in muscle fatigue. Lactate is an important intermediate in the process of wound repair and regeneration. The origin of elevated [lactate] in injury and sepsis is being re-investigated. There is essentially unanimous experimental support for a cell-to-cell lactate shuttle, along with mounting evidence for astrocyte-neuron, lactate-alanine, peroxisomal and spermatogenic lactate shuttles. The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic 'crimes', but is instead a central player in cellular, regional and whole body metabolism. Overall, the cell-to-cell lactate shuttle has expanded far beyond its initial conception as an explanation for lactate metabolism during muscle contractions and exercise to now subsume all of the other shuttles as a grand description of the role(s) of lactate in numerous metabolic processes and pathways.

Acidosis, Lactic↗
PubMed1986

Utilization of Lactate Isomers by Propionibacterium freudenreichii subsp. shermanii: Regulatory Role for Intracellular Pyruvate.

Five strains of Propionibacterium freudenreichii subsp. shermanii utilized the l-(+) isomer of lactate at a faster rate than they did the d-(-) isomer when grown with a mixture of lactate isomers under a variety of conditions. ATCC 9614, grown anaerobically in defined medium containing 160 mM dl-lactate, utilized only 4 and 15% of the d-(-)-lactate by the time 50 and 90%, respectively, of the l-(+)-lactate was used. The intracellular pyruvate concentration was high (>100 mM) in the initial stages of lactate utilization, when either dl-lactate or the l-(+) isomer was the starting substrate. The concentration of this intermediate dropped during dl-lactate fermentation such that when only d-(-)-lactate remained, the concentration was <20 mM. When only the d-(-) isomer was initially present, a similar relatively low concentration of intracellular pyruvate was present, even at the start of lactate utilization. The NAD-independent lactate dehydrogenase activities in extracts showed different kinetic properties with regard to pyruvate inhibition, depending upon the lactate isomer present. Pyruvate gave a competitive inhibitor pattern with l-(+)-lactate and a mixed-type inhibitor pattern with d-(-)-lactate. It is suggested that these properties of the lactate dehydrogenases and the intracellular pyruvate concentrations explain the preferential use of the l-(+) isomer.

Journal Article↗
PubMed1998

Lactate transport by cortical synaptosomes from adult rat brain: characterization of kinetics and inhibitor specificity.

Since lactate released by glial cells may be a key substrate for energy in neurons, the kinetics for the uptake of L-[U-14C]lactate by cortical synaptic terminals from 7- to 8-week-old rat brain were determined. Lactate uptake was temperature-dependent, and increased by 64.9% at pH 6.2, and decreased by 43.4% at pH 8.2 relative to uptake at pH 7.3. Uptake of monocarboxylic acids was saturable with increasing substrate concentration. Eadie-Hofstee plots of the data gave evidence of two carrier-mediated uptake mechanisms with a high-affinity Km of 0.66 mM and Vmax of 3.66 mM for pyruvate, and a low-affinity system with a Km of 9.9 mM for both lactate and pyruvate and Vmax values of 16.6 and 23.1 nmol/30 s/mg protein for lactate and pyruvate, respectively. Saturable uptake was seen in the presence of 10 mM alpha-cyano-4-hydroxycinnamate. Lactate transport by synaptic terminals was much more sensitive to inhibition by sulfhydryl reagents than transport in astrocytes. Addition of 0.5 and 2 mM mersalyl decreased the uptake of 1 mM lactate by synaptic terminals by 59.3 and 66.37%, respectively. Pyruvate moderately decreased lactate transport, whereas 3-hydroxybutyrate had little effect. Quercetin, an inhibitor of lactate release, had little effect on the content of 14C lactate in synaptic terminals, supporting the concept that the majority of lactate produced within brain is from glial cells. Oxidation of L-[U-14C]lactate by synaptosomes was saturable, and yielded a Km of 1.23 mM and a Vmax of 116 nmol/h/mg protein. Overall the studies show that synaptic terminals from adult brain have a high capacity for transport and oxidation of lactate, consistent with the proposed role for this compound in metabolic trafficking in brain. Furthermore, the data provide kinetic evidence of two carrier-mediated mechanisms for monocarboxylic acid transport by synaptosomes and demonstrate that uptake of lactate by synaptic terminals is regulated differently than transport by astrocytes. Uptake of lactate by synaptic terminals also has differences from the systems described for neurons.

Animals↗
PubMed1999

Lactate metabolism and glucose turnover in the subterranean crustacean niphargus virei during post-hypoxic recovery

Glucose and lactate metabolism were studied in a hypoxia-resistant subterranean crustacean, Niphargus virei, using an injection of l-[U-14C]lactate and tracer d-[6-3H]glucose either in normoxic conditions or after a 24 h exposure to severe hypoxic. Post-hypoxic animals (H animals) were compared with two treatment groups of normoxic animals. In the first normoxic group (NLL animals), animals were simultaneously injected with labelled and unlabelled lactate to obtain a lactate load similar to that of H animals. In the second normoxic group (N, control animals), animals were only injected with labelled lactate. During a 24 h recovery period, the incorporation of 14C and 3H into glycogen, lactate, glucose, amino acids, lipids and CO2 was measured. During recovery, glucose turnover rate was enhanced in H and depressed in NLL compared with N animals. However, when energy expenditure was taken into account, the changes were due only to a reduction of glucose turnover rate by lactate load. It was concluded that gluconeogenesis was not the main source of glyconeogenesis. Equivalent lactate loading in NLL and H animals resulted in an equivalent enhancement (fivefold) of lactate utilization in both groups when energy expenditure was taken into account. Lactate label incorporation appeared later in glycogen than in glucose, but remained high 24 h after the injection. Since glucose is mainly an extracellular metabolite, this observation may be consistent with the hypothesis of two distinct sites for glycogen restoration in hypogean crustaceans: a gluconeogenic organ (a liver equivalent) and a glyconeogenic organ (a muscle equivalent). The oxidative pathways of glucose and lactate were depressed in post-hypoxic N. virei and to a lesser extent in the NLL group. Since there is no evidence of marked protein utilization, it is postulated that, during recovery, repayment of the O2 debt relies on an increase in lipid utilization. During recovery from severe hypoxia or after a lactate load, the subterranean N. virei appeared to implement a strategy of lactate removal quite different from that observed in epigean crustaceans, favouring lactate-supported gluco- and glyconeogenesis and rapid glycogen replenishment instead of rapid lactate removal via oxidative pathways.

Journal Article↗
PubMed1998

Quality assessment of two lactate test strip methods suitable for obstetric use.

Accuracy of lactate determinations in cord blood was tested for one reflectometric (Accusport) and one amperometric (Lactate Pro) microvolume test strip lactate meter. Both meters, using a whole blood sample, measure lower levels of lactate than a reflectometric device considered as a reference method, which analyses lactate in plasma. Readings were unaffected irrespective of lactate concentrations for the Lactate Pro, whilst the Accusport overestimated low lactate concentrations and underestimated high values. Both lactate meters underestimated lactate concentrations at high hematocrits, as compared with the reference method. The Lactate Pro has a fixed sample volume of 5 microliters while the Accusport uses random blood drop as sample volume. However, in analyses with less than 20 microliters sample volume considerable underestimation was found with the Accusport. Coefficient of variation was 3.8-8.9% for the Accusport and 3.1-4.0% for the Lactate Pro within lactate concentrations between 2.1 and 5.3 mmol/l. The amperometric device, the Lactate Pro, performed best in these tests dealing with fetal blood lactate concentrations. The new technique can be a useful tool in perinatal research as well as in obstetric practice.

False Negative Reactions↗
PubMed2000

Lactate prevents the alterations in tissue amino acids, decline in ATP, and cell damage due to aglycemia in retina.

Under conditions of energy impairment, CNS tissue can utilize substrates other than glucose to maintain energy metabolism. Retinas produce large amounts of lactate, although it has not been shown that lactate can be utilized by retina to prevent the cell damage associated with hypoglycemia. To investigate this, intact, isolated retinas were subjected to aglycemic conditions in the presence or absence of 20 mM lactate. Retinas incubated in the absence of glucose for 60 min showed a threefold elevation in tissue aspartate and 60% decreases in tissue glutamate and glutamine, demonstrating a mobilization of carbon from glutamine and glutamate to the tricarboxylic acid cycle. Lactate prevented these changes in tissue amino acids, indicating metabolism of lactate with sparing of tissue glutamate and glutamine. Tissue ATP was 20 and 66% of control values with zero glucose or zero glucose plus lactate, respectively. Consistent with previous findings, incubation of retinas in the absence of glucose caused acute swelling of retinal neurons and release of GABA into the medium at 60 min. These acute toxic affects caused by the absence of glucose were completely prevented by the presence of lactate. At 24 h of recovery following 60 min of zero glucose, many pyknotic profiles were observed and lactate dehydrogenase (LDH) release into the medium was elevated sevenfold, indicating the extent of cell death. In contrast, no elevation in LDH was found and histology appeared normal in retinas exposed to zero glucose in the presence of lactate. alpha-Cyano-4-hydroxy cinnamate (4-CIN; 0.5 mM), an inhibitor of the monocarboxylic acid transporter and mitochondrial pyruvate carrier, blocked the ability of lactate to maintain ATP and protect retinas from aglycemia but had no effect on ATP or toxicity per se. Derangements in tissue aspartate, glutamate, and glutamine, which were prevented by lactate during zero glucose incubation, were again observed with lactate plus zero glucose in the presence of 4-CIN. However, 0.5 mM 4-CIN alone in the presence of glucose produced similar increases in aspartate and decreases in glutamate and glutamine as observed with zero glucose while having only modest inhibitory effects on [U-(14)C]lactate uptake, suggesting the mitochondrial pyruvate carrier as the main site of action. The above findings show that lactate is readily utilized by the chick retina during glucose deprivation to prevent derangements in tissue amino acids and ATP and retinal neuronal cell death.

Adenosine Triphosphate↗
PubMed1985

Roles of lactate and its interactions with acetate in maintenance and biosynthesis in bovine mammary tissue.

Mammary gland tissue slices from three lactating Holstein cows were incubated in Krebs-Ringer bicarbonate-based media with varying concentrations of lactate and other substrates. Conversions of 1- and 2-carbon-14 of lactate to carbon dioxide, fatty acids, citrate, glyceride glycerol, and lactose were determined. Effects of acetate, glucose, beta-hydroxybutyrate, stearate, and pyruvate on lactate metabolism were evaluated. Oxidation of lactate increased asymptotically with lactate concentration. Low acetate concentration stimulated oxidation of carbon 2 of lactate slightly while higher acetate availability inhibited lactate oxidation. Conversion of lactate to fatty acids increased linearly with lactate concentration. This conversion of lactate was inhibited strongly by acetate. Significant conversion of carbon 2 of lactate to glyceride-glycerol but not lactose was detected. Bovine mammary glands have the capacity of utilize sizeable quantities of lactate for oxidation and lipogenesis. Both phenomena are highly dependent on availability of acetate. Pyruvate dehydrogenase and citrate lyase could represent important regulatory sites in vivo for determination of tissue preference for acetate over lactate. Results indicate factors other than an inactive malate transhydrogenation cycle likely limit glucose conversion to fatty acids.

Acetates↗
PubMed2003

Combined hormonal versus nonhormonal versus progestin-only contraception in lactation.

BACKGROUND: Contraception for women who are breastfeeding is a public health issue of global importance. Each year over 100 million women make decisions about beginning or resuming contraception after childbirth. These decisions include both the choice of contraceptive method and the time at which its use begins, both of which continue to be debated by experts. Choices of contraception may be limited for lactating women due to concerns about hormonal effects on quality and quantity of milk, passage of hormones to the infant, and infant growth. Ideally, the contraceptive method chosen should not interfere with lactation. Additionally, because the return of menstruation and ovulation can be unpredictable in breastfeeding women, the timing of contraception initiation is important. OBJECTIVES: To determine the effect of combined oral contraceptives and progestin-only contraceptives on lactation. The a priori hypothesis is that combined oral contraception impairs lactation, making it less appropriate than progestin-only or nonhormonal contraception for breastfeeding women. SEARCH STRATEGY: We used PUBMED, POPLINE, EMBASE, LILACS, and Cochrane Controlled Trials Register computer searches, supplemented by review articles and contact with investigators. SELECTION CRITERIA: We sought all randomized controlled trials, reported in any language, that included any form of hormonal contraception compared with another form of hormonal contraception, nonhormonal contraception, or placebo during lactation. Hormonal contraception could include combined oral or injectable contraceptives, progestin-only oral or injectable contraceptives, hormonal implants, or hormonal intrauterine devices. Study participants included breastfeeding women of any age or parity who desired contraception. DATA COLLECTION AND ANALYSIS: We evaluated the methodological quality of each report and sought to identify duplicate reporting of data from multicenter trials. We abstracted data onto data collection forms. Principal outcome measures included quantity of milk; biochemical analysis of milk composition; initiation, maintenance and duration of lactation; infant growth; efficacy of contraceptive method while breastfeeding; and timing of contraception initiation and its effects on lactation. Because the trials did not have uniform interventions, often lacked quantifiable outcomes, and had poor methodological quality, we could not aggregate the data in a meta-analyses. MAIN RESULTS: Seven reports from five randomized controlled trials met our inclusion criteria. Most of the five trials did not specify their method used to generate a random sequence, method of allocation concealment, blinding of treatments, or use of an intention-to-treat analysis. Additionally, high loss to follow-up rates invalidated at least two studies. The findings from two reports comparing oral contraceptives to placebo during lactation were conflicting. Another trial found no inhibitory effects on lactation from progestin-only contraceptives. Finally, the WHO trial found no effect of progestin-only contraceptives on lactation but a decline in breast milk volume from combination contraceptives during lactation. High loss to follow-up rates, however, undermine the credibility of the WHO trial. No significant differences in infant growth or weight appeared in any of the included trials as a result of the use of hormonal contraception during lactation. REVIEWER'S CONCLUSIONS: Evidence from randomized controlled trials on the effect of hormonal contraceptives during lactation is limited and of poor quality; results should be interpreted with caution. The existing randomized controlled trials are insufficient to establish an effect of hormonal contraception, if any, on milk quality and quantity. Evidence is inadequate to make recommendations regarding hormonal contraceptive use for lactating women. At least one properly conducted randomized controlled trial of adequate size is urgently needed to address this question.

Contraceptives, Oral, Combined↗
PubMed1989

The 1H NMR visibility of intracellular lactate in Streptococcus faecalis.

1H NMR studies of glycolysis in washed cell suspensions of Streptococcus faecalis indicated that intracellular lactate is not 1H NMR visible. Evidence for this was gained from time course studies of glycolysis at increasing concentrations of glucose. A close correlation existed between the relative increase in the lactate integral and the enzymatically determined extracellular lactate concentration [Lo]. When ionophores which cause the collapse of the positive intracellular/extracellular lactate gradient were added to cell suspensions following fermentation of 5, 10 and 50 mM glucose, the increase in the lactate integral was proportional to the respective increase in [Lo]. A more direct method for determining the origin of the lactate signal involved centrifugation of a cell suspension after fermentation of 50 mM glucose and measurement of lactate in the extracellular and intracellular fluid. 1H spectra of the cell suspension, supernatant and sonicated pellet revealed that the lactate observed in the cell suspension was equivalent to the lactate in the supernatant alone. The intracellular lactate contained in the pellet represented 42% of the total lactate, indicating that only 58% of lactate is detected by in vivo 1H MRS of S. faecalis. This result is in contrast with the high percentage (70-90%) of in vitro lactate which is detected by in vivo 1H MRS of mammalian brain tissue (Williams S. R. et al. Magn. Res. Med. 7, 425-431, 1988). This may be due to a higher proportion of extracellular lactate in mammalian tissue or differences in the intracellular environments of bacterial and mammalian cells.

Enterococcus faecalis↗
PubMed1994

Trans-stimulation of lactate transport from rat sarcolemmal membrane vesicles.

We examined the trans-stimulation characteristics of L(+)-lactate efflux from rat skeletal muscle sarcolemmal membrane vesicles isolated by sucrose density gradient centrifugation. Vesicles were preloaded with 1 mM L(+)-lactate containing 14C tracer lactate. Initial efflux of intravesicular lactate was stimulated above baseline efflux by the presence of 30, 50, or 100 mM L(+)-lactate in the external medium; resulting efflux rates were 120, 138, and 141% of baseline values, respectively. Extravesicular pyruvate (100 mM) stimulated efflux to only 110% of baseline, while unlabeled D(-)-lactate in the external medium did not stimulate lactate efflux. Trans-stimulation of L(+)-lactate efflux in response to extravesicular lactate exhibited saturation kinetics. We conclude that the sarcolemmal lactate transporter is stereospecific for L(+)-lactate; pyruvate can share the transporter, although the affinity of the transporter for pyruvate is less than that for L(+)-lactate. Furthermore, because the presence of lactate on one side of the sarcolemma stimulates transport from the opposite side, the transporter is not likely to be a pore or channel, but rather this carrier probably undergoes a conformational change as it translocates lactate from one membrane side to the other.

Animals↗
PubMed1990

Lactate transport is mediated by a membrane-bound carrier in rat skeletal muscle sarcolemmal vesicles.

To study the kinetics of lactate transport in an isolated, nonmetabolizing system, skeletal muscle sarcolemmal membrane vesicles were purified from 22 female Sprague-Dawley rats. L(+)-[U-14C] Lactate at 10 concentrations demonstrated saturation kinetics with a Vmax of 139.4 nmol/mg/min, and an apparent Km of 40.1 mM. Threefold higher initial rates of L(+)-lactate uptake were seen at 37 degrees C than at 25 degrees C, indicating temperature sensitivity. Transport was stereospecific for the L(+) isomer: isotopic D(-) uptake rates remained linear at concentrations from 1 to 200 mM, and 1 mM D(-) remained 6-fold lower in net uptake after 60 min than the L(+) isomer. Furthermore, unlabeled 10 mM D(-)-lactate in the external medium could only inhibit 1 mM isotopic (L(+) uptake by 12%, whereas unlabeled 10 mM L(+)-lactate and pyruvate inhibited 82 and 71%, respectively. Additionally, 10 mM beta-hydroxybutyrate and acetoacetate could moderately inhibit (27 and 32%, respectively) 1 mM L(+)-lactate transport, but the unsubstituted aliphatic monocarboxylates (formate, acetate, propionate), tricarboxylic acid cycle intermediates (malate, succinate, oxaloacetate, alpha-ketoglutyrate, citrate), amino acids (alanine, aspartate, glutamate), and palmitate or adenosine in 10-fold excess could not effectively inhibit 1 mM L(+)lactate uptake under cis-transport conditions. 4,4'-Diisothiocyanostilbene-2,2'-disulfonic acid could inhibit L(+)-lactate transport by only 13%, so that lactate transport does not appear to be affected directly by Cl- or HCO3- fluxes. It was demonstrated that KCl could not evoke a membrane potential-induced overshoot of lactate uptake in the presence or absence of valinomycin. Moreover, gluconate could substitute for Cl-, indicating that Cl- flux does not contribute to a membrane potential-dependent component of the transport mechanism, suggesting an electroneutral translocation process. Protein-modifying reagents significantly inhibited 1 mM L(+)-lactate transport during pH-stimulated conditions (p-chloromercuriphenyl-sulfonic acid, 83%; N-ethylmaleimide, 86%; HgCl2, 56%; mersalyl, 63% inhibition). We conclude that the skeletal muscle lactate transporter is a membrane-bound protein, specifically associated with the sarcolemma, that demonstrates saturation kinetics, competition, stereospecificity, and sensitivity to temperature as well as various ionic cis-inhibitors. The lactate transporter is a potentially important regulator of lactate flux across skeletal muscle, and may help to regulate intracellular pH and intermediary metabolism during lactic acidosis.

Animals↗
PubMed2005

Lactation weight loss influences subsequent reproductive performance of sows.

UNLABELLED: In order to examine the effect of different lactation weight losses of sows of different parity on subsequent reproductive performance, the present trial was performed in German (n = 4) and Slowakian (n = 11) indoor pig breeding units (n = 1677 sows evaluated). Weaning-to-service-intervals, farrowing rates and total-born litter sizes in sows with different lactation weight losses were compared. Sows were categorized according to lactation weight losses of <5%, 5-10%, 11-15%, 16-20%, >20%. Lactation weight losses exerted a quadratic effect (P < 0.01) on weaning-to-service-intervals. When analyzed across parity categories, with parity category included as a fixed effect, the weaning-to-service-intervals appeared to be minimized at lactation weight losses of <5%. Weaning-to-service-intervals increased (P < 0.05) when lactation weight losses increased above 5% for parity 1 sows, but not until lactation weight losses exceeded 10% for animals of parity 2 and more. There was a parity effect observed at lactation weight losses of <10%, P < 0.05, but the difference was not significant any more at lactation weight losses of >10%. Lactation weight losses >10% had a negative (P < 0.05) effect on subsequent farrowing rates to first service. The difference was higher (P < 0.01) in sows with lactation weight losses >20%. Lactation weight losses exerted a negative (P < 0.001) effect on total-born litter sizes in parity 1 versus parity >5 and parity 1 versus parity 2-5 sows at lactation weight losses of >10%. CONCLUSION: As weight loss of sows during lactation increases subsequent reproduction performance decreases.

Animals↗
PubMed1997

Lactation decreases mRNA levels of opioid peptides in the arcuate nucleus of the rat.

The state of lactation results in increased food intake to compensate for the increased energy expenditure to produce nutrients supplied to the offspring. In this study, Sprague-Dawley female rats lactating for 10-16 days, and rats 7 days post-lactation were implanted with osmotic minipumps infusing either naltrexone (NTX) (70 microg/h) or saline (0.9%) over a 48 h period. mRNA levels of pro-dynorphin (proDYN), pro-opiomelanocortin (POMC) and pro-enkephalin (proENK) were measured in the arcuate nucleus (ARC) and whole pituitary of both groups. In both saline- and NTX-treated lactating subjects, food intake was higher than in post-lactating subjects (P < 0.01). In post-lactating subjects, NTX decreased food intake by 27% during the infusion period (P < 0.05). There were no significant differences in body weight between the treatment groups; however, naltrexone decreased body weight gain in both lactating and post-lactating subjects. In both saline and NTX-treated lactating subjects, ARC mRNA levels of proDYN, POMC and proENK were significantly decreased compared with the saline or NTX-treated post-lactating subjects (P < 0.01). NTX did not significantly influence gene expression of opioid peptides in the ARC in either the lactating or the post-lactating subjects. Neither the lactation condition nor NTX administration significantly changed mRNA levels of proDYN, POMC or proENK in whole pituitary. Thus, as has been noted in energy-deprived rats, opioid peptide gene expression is decreased in the ARC of lactating rats, a period during which rats have increased energy requirements.

Animals↗
PubMed2001

Decreased number and bactericidal activity against Staphylococcus aureus of the resident cells in milk of dairy cows during early lactation.

Phagocytic and bactericidal activity of polymorphonuclear neutrophil leukocytes (PMN) isolated from blood and milk, against Staphylococcus aureus, was compared between groups of six healthy dairy cows in early, mid- and late lactation using a bacteriological assay. PMN were isolated from blood with a high degree of purity, but the cells isolated from milk contained variable amounts of macrophages (Mphi) and lymphocytes (L). The results were therefore calculated using the percentage PMN in order to evaluate phagocytosis and killing by PMN only. Blood PMN phagocytosed 82% Staph. aureus and milk PMN 43% on average and there was no significant difference between the different stages of lactation. The bactericidal activity of blood PMN against Staph. aureus was 36+/-8% in early lactation (significantly different from mid lactation, P < 0.05), 64+/-10% in mid lactation and 53+/-6% in late lactation. Milk PMN killed only 6+/-3% Staph. aureus in early lactation (significantly different from mid lactation, P < 0.01), 27+/-3% in mid lactation and 20+/-9% Staph. aureus in late lactation. The ratio of the bactericidal activity of milk to blood PMN was 0.08, 0.43 and 0.22 in early, mid- and late lactation, respectively. In addition to the decreased function. the number of cells in milk (somatic cell count, SCC) was also 60% lower in early lactation than in mid lactation cows (P < 0.01). Our results suggest an impairment of blood and milk-resident PMN bactericidal activity against Staph. aureus and a decreased number of milk-resident PMN in dairy cows at the onset of lactation.

Animals↗
PubMed2002

Mammary apoptosis and lactation persistency in dairy animals.

The decline in milk yield after peak lactation in dairy animals has long been a biological conundrum for the mammary biologist, as well as a cause of considerable lost income for the dairy farmer. Recent advances in understanding the control of the mammary cell population now offer new insights on the former, and a potential means of alleviating the latter. The weight of evidence now indicates that a change in mammary cell number, the result of an imbalance between cell proliferation and cell removal, is a principal cause of declining production. Further, it suggests that the persistency of lactation, the rate of decline in milk yield with stage of lactation, is strongly influenced by the rate of cell death by apoptosis in the lactating gland. Mammary apoptosis was first demonstrated during tissue involution after lactation, but has now been detected during lactation, in mammary tissue of lactating mice, goats and cattle. Those factors that determine the rate of cell death by apoptosis are as yet poorly characterized, but include the frequency of milking in lactating goats. Initial evidence suggests that nutrition also is likely to influence cell survival after peak lactation, an important factor being the degree of oxidative stress imposed by feed and the tissue's ability to deal with, and prevent damage by, reactive oxygen species. Comparison of cows in calf or not pregnant during declining lactation also indicates a likely influence of reproductive hormones, with oestradiol and progesterone acting to preserve mammary ductal and alveolar integrity during the dry period, while allowing a degree of apoptosis and cell replacement. In each case, the molecular mechanisms controlling mammary cell survival (or otherwise) are as yet poorly defined. On the other hand, more persistent lactations are likely to benefit animal welfare through fewer calvings and by placing less emphasis on maximal production at peak lactation, and modelling of persistent lactation with longer calving intervals indicates their likely economic benefits. In these circumstances, there is considerable incentive to elucidate the determinants of mammary apoptosis, and the factors controlling the dynamic balance between cell proliferation and cell death in the lactating mammary gland.

Animal Nutritional Physiological Phenomena↗