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PubMed1995

Stimulated thyrotropin and prolactin secretion in lactating and non-lactating women.

During the postpartum period, lactation is initiated by a massive release of prolactin which, in turn, reflects reduced dopaminergic inhibition of the pituitary lactotrophs. This postpartum prolactin rise can be prevented by administration of dopamine agonists. The release of thyrotropin (TSH) is also controlled by dopaminergic inputs and, therefore, TSH secretion may also be affected by postpartum alterations in dopaminergic activity. To gain further insight into the regulation of TSH and prolactin secretion during the postpartum period, we compared the basal and stimulated TSH and prolactin levels of postpartum lactating (n = 10) and non-lactating women (treated with 5 mg bromocriptine daily, n = 9) with those of normal cycling women (n = 9). Frequent blood samples were obtained on postpartum day 5 or in the early follicular phase before and after administration of thyrotropin-releasing hormone (TRH) for serial determination of TSH and prolactin by immunoradiometric assay (IRMA). Based serum prolactin levels were high (p < 0.001) in lactating women and low in both non-lactating and normal cycling women. When these differences in the basal prolactin concentrations were taken into account, the stimulated prolactin release (relative prolactin increase and area under the prolactin curve) was found to be highest (p < 0.05) in non-lactating women and lowest in lactating women. Basal TSH secretion was not significantly different between the groups of women (p > 0.2). Yet, both the relative TSH increases and the response curves following TRH stimulations were high (p < 0.05) in normal cycling women and low in both lactating and non-lactating postpartum women. These observations confirm a difference in the basal and stimulated prolactin release between lactating and non-lactating women. They also indicate that the TRH-stimulated TSH release is greatly affected by the postpartum state, irrespective of lactation or therapeutic weaning. The observation of a decreased sensitivity of pituitary thyrotrophs in concert with unchanged basal TSH secretion is suggestive of changes in hypothalamic TRH secretion and/or in the TSH metabolic half-life during the postpartum period.

Adult↗

PubMed2006

Productive life including all lactations and longer lactations with diminishing credits.

Alternative measures of productive life (PL) were compared, and life expectancy factors were updated to replace estimates from 1993. Alternatives were proposed with extra credits for lactations longer than 10 mo and beyond 84 mo of age and for each calving so that an extremely long lactation would not receive more credits than multiple shorter lactations with dry periods between. Maximum credits per lactation of 10 mo (original PL), 12 mo, and unlimited were compared. The unlimited credits option either included or excluded a calf value equal to 2 mo of production and had credits given for all days either uniformly or based on lactation curves (diminishing credits). Standard lactation curves (first, second, and greater lactations) were estimated based on the test-day yields of Holstein cows remaining in lactation from a set of 903,579 lactation records. For the diminishing credits alternative, credit for a given day of a parity was derived using the predicted yield of the day proportional to the average daily yield of the first 305 d of second parity. Daily yields were deviations from a baseline of 13.62 kg. Heritabilities and genetic correlations were estimated by multitrait REML for alternative measures of PL, for longevity censored at various ages, and for yield traits and SCS in first parity. Data for REML analysis included records from 1,098,329 Holsteins born from 1994 through 1997 from 5,109 sires, and a relationship matrix among sires was included in the model. Lactations beyond 84 mo added little information. Heritability of PL was 0.073 with 10 mo, 0.069 with 12 mo, 0.068 and 0.067 with unlimited (uniform) lactation credits (with and without calf credits, respectively), and 0.070 with unlimited diminishing credits. Corresponding correlations among predicted transmitting abilities for PL and protein yield were 0.07, 0.06, 0.12, 0.23, and 0.09, all much lower than the 0.46 estimated in 1993. Heritability of PL with diminishing credits improved from 0.017 to 0.070 when censoring age increased from 36 to 96 mo. There was no further increase in heritability beyond 96 mo. Genetic correlation with the final PL was 0.87 when PL was censored at 36 mo, but the estimate increased steadily with the censoring age. The PL with diminishing credits, which was favorable in both economic and genetic aspects, was desirable in crediting cows for complete lactations.

Aging↗

PubMed2000

Evaluation of the Lactate Pro blood lactate analyser.

An evaluation of the hand-held portable Lactate Pro Analyser (KDK) was undertaken to assess its accuracy, reliability and versatility. Capillary blood samples were drawn from elite athletes in both laboratory and field settings and analysed in parallel. Accuracy was determined in relation to three other lactate analysers: (1) the ABL 700 Series Acid-Base analyser (n = 172 cases), (2) the Accusport Lactate Meter (n = 118 cases), and (3) the YSI 2300 Stat lactate analyser (n = 22 cases). The level of agreement was determined over the range of 1-18 mM. The repeatability of results between two different Lactate Pro analysers was also determined over the same range. Versatility was assessed in the field, where the Lactate Pro was used with elite athletes under a range of outdoor and indoor testing conditions. The correlations between the Lactate Pro and the ABL 700 Series Acid-Base analyser, YSI 2300 and Accusport were r = 0.98, r = 0.99, r = 0.97. The correlation between the two Lactate Pro analysers on the same sample (n = 96 cases) was r = 0.99. The level of agreement between the Lactate Pro and other analysers was generally less than +/- 2.0 mM over the physiological range of 1.0-18.0 mM (range of mean difference: -0.06 mM to 0.52 mM). The Lactate Pro was easy to operate and successfully completed the sample analysis in 100% of the tests performed. In summary, the Lactate Pro is accurate, reliable and exhibits a high degree of agreement with other lactate analysers.

Adolescent↗

PubMed1973

Reconstitution of D-lactate-dependent transport in membrane vesicles from a D-lactate dehydrogenase mutant of Escherichia coli.

Membrane-bound, flavin-linked D-lactate dehydrogenase in membrane vesicles of E. coli ML 308-225 is solubilized by extraction with guanidine HCl. When membrane vesicles prepared from a D-lactate dehydrogenase mutant are treated with this extract, they regain the capacity to catalyze D-lactate oxidation and D-lactate-dependent transport. Similar effects are obtained with wild-type membrane vesicles in which D-lactate oxidation and D-lactate-dependent transport have been inactivated by 2-hydroxy-3-butynoate. Although treatment of wild-type vesicles with the extract results in an increased capacity to catalyze D-lactate oxidation, no effect on transport is observed. Reconstituted transport activity is a saturable function of the amount of guanidine extract added. Moreover, the quantity of extract required to achieve maximum initial rates of transport varies with each transport system. On the other hand, reconstituted D-lactate oxidation increases linearly over a broader range of extract concentrations.Oxamate, a competitive inhibitor of D-lactate dehydrogenase, and p-chloromercuribenzenesulfonate block both the initial rate of transport and the steady-state level of accumulation in reconstituted vesicles. Furthermore, these reagents induce efflux of transport substrates from preloaded, reconstituted vesicles. The same reagents inhibit the initial rate of uptake but not the steady-state level of accumulation in ML 308-225 vesicles, and do not induce efflux. These results suggest that, although reconstituted vesicles catalyze D-lactate oxidation and D-lactate-dependent transport, the system has not been reconstituted to its native state.

Amino Acids↗

PubMed2000

Changes in leptin levels during lactation: implications for lactational hyperphagia and anovulation.

In these studies we investigated the time course of changes in circulating leptin levels in lactating rats and the dependence of these changes on the energetic cost of lactation and evaluated the contribution of changes in leptin levels to lactational hyperphagia and infertility. In the first experiment, plasma leptin levels were measured on Days 5, 10, 15, 20, and 25 postpartum in freefeeding lactating rats and age-matched virgin females. Retroperitoneal and parametrial fat pads weights were obtained from the same females. In the second experiment the same measures, together with plasma insulin and prolactin levels, were taken on Days 15 and 20 postpartum from galactophore-cut and sham-operated females. In Experiments 3 and 4, the effects of exogenous leptin administration, either subcutaneously (sc) or intracerebroventricularly (icv), on lactational anovulation, maternal food intake, and dam and litter weights were examined. Circulating leptin levels decreased in lactating rats. Leptin levels were highly positively correlated with fat pad weight. Eliminating the energetic costs of lactation by preventing milk delivery induced dramatic increases in plasma leptin and insulin levels and also increased adiposity. Exogenous leptin administration did not affect length of lactational anovulation but reduced food intake, maternal body weight, and litter weight gain when given centrally and maternal body weight when given systemically. Together, these data show that the energetic costs of lactation are associated with a fall in circulating leptin levels but that these do not make a major contribution to the suppression of reproduction in lactating rats; however, they may be permissive to the hyperphagia of lactation.

Animals↗

PubMed2001

No difference in net uptake or disposal of lactate by trained and untrained forearms during incremental sodium lactate infusion.

A number of training adaptations in skeletal muscle might be expected to enhance lactate extraction during hyperlactataemia. The aim of the present study was to determine whether resting endurance-trained forearms exhibit an increased net lactate removal during hyperlactataemia. Six racquet-sport players attended the laboratory for two experiments, separated by 2 weeks. In the first experiment incremental handgrip exercise to fatigue was performed to identify trained (TRFA, n = 6) and untrained (UTFA, n = 5) forearms. In the second experiment net forearm lactate exchange was compared between TRFA and UTFA during an incremental infusion of sodium lactate. TRFA performed more work than UTFA during handgrip exercise [mean (SE) TRFA, 66.1 (9.5) J.100 ml(-1); UTFA, 35.1 (2.3) J.100 ml(-1); P = 0.02] and UTFA exhibited a greater increase in net lactate output relative to work load (P = 0.003). During lactate infusion net lactate uptake across the resting forearms increased linearly with the arterial lactate concentration in both groups (TRFA, r = -0.95 (0.03); UTFA, r= -0.92 (0.04); P < 0.02], with no difference in the regression slopes [TRFA, -1.06 (0.13); UTFA, -1.07 (0.27); P = 0.97] or y-intercepts [TRFA, 0.67 (0.20); UTFA, 1.36 (0.67); P = 0.37] between groups. Almost all of the lactate taken up was disposed of by both groups of forearms [TRFA, 99.6 (0.2)%; UTFA, 98.5 (1.0)%; P = 0.37]. It was concluded that the net uptake and removal of lactate by resting skeletal muscle is a function of the concentration of lactate in the blood perfusing the muscle rather than the muscle training status.

Adult↗

PubMed1989

Lactate extraction fails to accurately reflect regional lactate production in ischemic myocardium.

Lactate extraction (defined as arteriovenous lactate concentration difference divided by arterial concentration and expressed as a percent) is often reported as the indicator of anaerobic cardiac metabolism in studies dealing with myocardial ischemia. However, lactate extraction ignores the effect of regional blood flow and, therefore, fails to consider the total mass of lactate consumed or produced (lactate flux). This study examined the relationship between lactate flux and calculated lactate extraction. Fourteen anesthetized dogs were instrumented to allow sampling of blood from the left anterior descending coronary artery (LADa) and vein (LADv) and a circumflex coronary vein (CFXv), as well as measurement of regional myocardial blood flow (RMBF) using microspheres, and measurement of systemic hemodynamic variables. Complete data sets (before LADa occlusion, after 15 minutes of LAD occlusion, and after 1 hour of reperfusion) were obtained in nine dogs. Only minor systemic hemodynamic changes occurred during LADa occlusion when compared with "before" and "after" values. Likewise, LADa occlusion produced only minor alterations in blood gas tensions, pH, concentrations of glucose, lactate, and RMBF in samples from the CFX perfusion zone. In contrast, LAD occlusion decreased RMBF in the LADa perfusion zone and produced significant hypercarbia and acidemia, as well as an increased LADv lactate concentration. In the LAD zone, lactate extraction decreased significantly from 15.9% +/- 7.0% before LAD occlusion to -77.4% +/- 21.8% during LAD occlusion (P less than 0.05). However, lactate flux (arteriovenous concentration difference x RMBF) in the LAD zone before and during LAD occlusion was not statistically significantly different (1.3 +/- 0.8 mg/min/100 g and -1.5 +/- 0.8 mg/min/100 g, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Amperometric lactate oxidase catheter for real-time lactate monitoring based on thin film technology.

An amperometric lactate oxidase catheter has been developed for in vivo application to real-time lactate monitoring. The electrochemical behaviour of the 1 x 3 mm Pt-Ag/AgCl thin film electrode is not significantly influenced by lactate oxidase-polyurethane covering. Gamma-irradiation (25 kGy) is suitable for the sterilization procedure. The final lactate catheter is characterized by a linear concentration range between 0.5 and 20 mmol/l lactate with a sensitivity around 2 nA mmol-1 l-1 lactate. The accuracy is demonstrated by the measurement of control sera. Both physiological and pathological materials correlate well with the declared values. The dry stored lactate catheter needs about 10 min for hydration and is characterized by response times t98% of less than 2 min. Ex vivo whole blood measurements using the lactate catheter (y) give a correlation with the BIOSEN Med L (x) of y = (1.010x + 0.513) mmol/l (r = 0.9748). Lactate values obtained by continuous catheter operation ex vivo correlate well with those obtained by BIOSEN Med L. First subcutaneous implantation (dog) underlines the characteristics obtained ex vivo: after 30 min hydration the lactate catheter follows the lactate concentration measured ex vivo with samples from the leg vein by BIOSEN Med L.

Animals↗

PubMed2000

In a medium containing glucose, lactate carbon is incorporated by gonococci predominantly into fatty acids and glucose carbon incorporation is increased: implications regarding lactate stimulation of metabolism.

The reason for stimulation by lactate of metabolism of gonococci growing in a medium containing glucose, which enhances pathogenicity by increasing growth rate, lipopolysaccharide (LPS) synthesis and protein formation, has been investigated. Tricine dodecylpolyacrylamide gel electrophoresis (SDS-PAGE) and thin layer chromatography (TLC) on homogenates of gonococci grown in this medium with [14C]lactate showed that lactate carbon was preferentially incorporated into lipid and LPS. Nuclear magnetic resonance (NMR) spectroscopy on lipid extracted from gonococci grown in the glucose containing medium with [13C]lactate showed that lactate carbon was incorporated into fatty acid moieties and not into ethanolamine or glycerol moieties. In contrast, NMR on lipid from gonococci grown with [13C]glucose indicated glucose carbon in both moieties. When unlabelled lactate was added, lipid synthesis from [l3C]glucose was stimulated and small amounts of different fatty acids were formed. The NMR data shows that gluconeogenesis from lactate carbon does not occur in the presence of glucose, suggesting that lactate is used solely for rapid production, via pyruvate, of acetyl CoA, the precursor not only for fatty acid synthesis but also for the constituents and products of the citric acid cycle, including ATP. The rapid formation of a high level of acetyl CoA is the probable reason for the stimulation of metabolism and oxygen uptake by lactate. 14C label on LPS was detected in its fatty acids. Most proteins that stained with silver in tricine SDS-PAGE were not significantly labelled by [14C]lactate in the glucose-containing medium. Two of three appreciably labelled proteins were identified by N-terminal sequencing as GroEL and porin 1B, and one of the two less labelled proteins was similar to peroxiredoxin type proteins. There were no signs of specific induction of these proteins by lactate and their labelling was consistent with fatty acids in attached lipid.

Bacterial Proteins↗

PubMed1989

Effects of lactate on pancreatic islets. Lactate efflux as a possible determinant of islet-cell depolarization by glucose.

The secretion of insulin from perifused rat pancreatic islets was stimulated by raising the glucose concentration from 5.6 to 20 mM or by exposure to tolbutamide. The addition of sodium lactate (40 mM) to islets perifused in the presence of glucose (5.6 mM) resulted in a small, transient, rise in the rate of secretion. The subsequent removal of lactate, but not glucose or tolbutamide, from the perifusate produced a dramatic potentiation of insulin release. The rate of efflux of 45Ca2+ was also increased when islets were exposed to a high concentration of glucose or lactate or to tolbutamide, and again subsequently upon withdrawal of lactate. Efflux of 86Rb+ was modestly inhibited upon addition of lactate and markedly enhanced by the subsequent withdrawal of lactate from islets. The output of [14C]lactate from islets incubated in the presence of [U-14C]glucose increased linearly with increasing concentrations of glucose (1-25 mM). It is proposed that the activation of islets by the addition or withdrawal of lactate is not due to increased oxidative flux, but occurs as a result of the electrogenic passage of lactate ions across the plasma membrane, resulting in islet-cell depolarization, Ca2+ entry and insulin secretion. The production of lactate via the glycolytic pathway, and the subsequent efflux of lactate from the islet cells with concomitant exchange of H+ for Na+, could be a major determinant of depolarization and hence insulin secretion, in response to glucose.

Animals↗

PubMed1992

Metabolism of pregnant-lactating rats is adapted to pregnancy rather than to lactation.

In pregnant-lactating rats implantation was induced on day 4 of lactation so that, as an exception, lactation coincided with the period of high fetal growth. The already present suckling litters of these animals lagged behind in growth, but the "second" litters were at birth normal in size and weight. Such pregnant-lactating rats were tested in vivo with intravenous glucose loads and compared with cyclic and lactating rats. Glucose tolerance was unaffected by the reproductive state. Pregnant-lactating rats showed, just as during their first pregnancy, low basal glucose levels. Their basal insulin levels and insulin responses, however, were decreased in comparison with the first pregnancy and resembled those of lactating rats. This may be due to an increased insulin turnover, because in vitro insulin responsiveness and insulin content of both "pregnant-lactating" and "pregnant" islets were increased in comparison with "cyclic" and "lactating" islets. It was concluded that the metabolism of pregnant-lactating rats is adapted to the pregnant rather than to the lactational state.

Adaptation, Physiological↗

PubMed1985

Lactate, pyruvate, and lactate-to-pyruvate ratio during exercise and recovery.

The pattern of lactate increase and its relation to pyruvate and lactate-to-pyruvate (L/P) ratio were studied during exercise and early recovery in 10 normal subjects for incremental exercise on a cycle ergometer. Gas exchange was measured breath by breath. Lactate and pyruvate were measured by enzymatic techniques. Lactate and log lactate changed only slightly at low levels of O2 uptake (VO2) but both began to abruptly increase at approximately 40-55% of the maximal VO2. However, the point of abrupt increase in pyruvate occurred at higher work rates and the rate of increase was not as great as that for lactate. Thus L/P ratio increased at the same VO2 as the log lactate increase. Following the exercise, pyruvate continued to increase steeply for at least the first 5 recovery min, whereas at 2 min lactate increased only slightly or decreased. Thus arterial L/P ratio reversed its direction of change and decreased toward the resting value by 2 min of recovery. Lactate, as well as L/P ratios, decreased in all subjects by 5 min. This study demonstrates that lactate and pyruvate concentrations increase slightly at low levels of exercise without a change in L/P ratio until a threshold work rate at which lactate abruptly increases without pyruvate. The resulting increase in L/P ratio is progressive as work rate is incremented and abruptly reverses when exercise stops.

Adult↗

PubMed2004

Diurnal rhythm of cerebrospinal fluid and plasma leptin levels related to feeding in non-lactating and lactating rats.

Leptin suppresses food intake and increases energy expenditure in the hypothalamus. Rats consume most of their daily food intake during the dark phase of the diurnal cycle. Lactating rats have increased food intake, but the involvement of leptin in the regulation of food intake in this physiological condition is not well understood. The present experiment was carried out to determine the circadian pattern of leptin concentrations in plasma and cerebrospinal fluid (CSF) in relation to the feeding behavior of non-lactating and lactating rats. Female rats were maintained on a controlled lighting schedule (lights on between 0600 and 1800 h) and the food intake of lactating rats was two- or threefold higher than that of non-lactating rats. In both groups, food intake was three times greater in the dark phase (P<0.01) compared with the light phase. The plasma concentrations of leptin were lower (P<0.01) in lactating rats than non-lactating rats in both light and dark phases, but there were no differences in plasma leptin levels between light and dark phases. In contrast, and in both groups, the leptin concentrations in CSF were lower (P<0.01) in the dark phase than in the light phase. Leptin levels in CSF were lower (P<0.01) in lactating rats than in non-lactating rats. We conclude that a diurnal pattern of leptin levels within the brain (but not in plasma) reflects characteristics of feeding behavior in lactating and non-lactating rats.

Animals↗

PubMed2000

Impaired expression of the uncoupling protein-3 gene in skeletal muscle during lactation: fibrates and troglitazone reverse lactation-induced downregulation of the uncoupling protein-3 gene.

The expression of uncoupling protein (UCP)-3 mRNA in skeletal muscle is dramatically reduced during lactation in mice. The reduction in UCP-3 mRNA levels lowers the amount of the UCP-3 protein in skeletal muscle mitochondria during lactation. Spontaneous or abrupt weaning reverses the downregulation of the UCP-3 mRNA but not the reduction in UCP-3 protein levels. In lactating and virgin mice, however, fasting increases UCP-3 mRNA levels. Changes in UCP-3 mRNA occur in parallel with modifications in the levels of free fatty acids, which are reduced in lactation and are upregulated due to weaning or fasting. Modifications in the energy nutritional stress of lactating dams achieved by manipulating litter sizes do not influence UCP-3 mRNA levels in skeletal muscle. Conversely, when mice are fed a high-fat diet after parturition, the downregulation of UCP-3 mRNA and UCP-3 protein levels due to lactation is partially reversed, as is the reduction in serum free fatty acid levels. Treatment of lactating mice with a single injection of bezafibrate, an activator of the peroxisome proliferator-activated receptor (PPAR), raises UCP-3 mRNA in skeletal muscle to levels similar to those in virgin mice. 4-chloro-6-[(2,3-xylidine)-pirimidinylthio] acetic acid (WY-14,643), a specific ligand of the PPAR-alpha subtype, causes the most dramatic increase in UCP-3 mRNA, whereas troglitazone, a specific activator of PPAR-gamma, also significantly increases UCP-3 mRNA abundance in skeletal muscle of lactating mice. However, in virgin mice, bezafibrate and WY-14,643 do not significantly affect UCP-3 mRNA expression, whereas troglitazone is at least as effective as it is in lactating dams. It is proposed that the UCP-3 gene is regulated in skeletal muscle during lactation in response to changes in circulating free fatty acids by mechanisms involving activation of PPARs. The impaired expression of the UCP-3 gene is consistent with the involvement of UCP-3 gene regulation in the reduction of the use of fatty acids as fuel by the skeletal muscle and in impaired adaptative thermogenesis, both of which are major metabolic adaptations that occur during lactation.

Animals↗

PubMed1985

Effect of bull selection for somatic cell count in first lactation on cell counts and pathogens in later lactations.

Somatic cell counts were measured one time on Meuse-Rhine-Ijssel cattle in The Netherlands. Experiment 1 involved 1,741 first lactation daughters of 31 bulls. Eleven bulls with daughters with either high or low average cell count were selected for further study of their daughters in third and fourth lactation. Cell counts and bacteriological tests were performed on 684 of the older daughters. A second experiment was conducted to measure daughters in second lactation and to obtain additional daughters in first lactation. This experiment recorded cell counts of 1,071 daughters of 10 of the bulls selected in Experiment 1. Heritability of the natural logarithm of cell count in first lactation was .081 based on daughters of 31 bulls in Experiment 1. Geometric daughter averages ranged from 206 to 700 X 10(3) cells/ml. Transmitting ability of bulls was estimated by the regressed least squares method. Ranking of bulls on first lactation cell count was different between the two experiments. Management factors and stage of lactation effects could be responsible for these differences. Within Experiment 2, the ranking of bulls on cell counts was nearly identical between first and second lactation. Daughter groups with low average cell count in first lactation in Experiment 2 had low averages in third and fourth lactation although some changes in ranking did occur. These results are consistent with a low to moderate genetic correlation between lactations for cell count. In general, daughter groups with higher average cell count had higher percentage of quarters with mastitis pathogens.

Animals↗

PubMed1980

Cyclic AMP regulation of lactate dehydrogenase. Isoproterenol and N6,O2'-dibutyryl cyclic AMP increase the levels of lactate dehydrogenase-5 isozyme and its messenger RNA in rat C6 glioma cells.

The mechanism of isoproterenol and N6,O2'-dibutyryl adenosine 3':5'-monophosphate (dibutyryl cAMP) induction of lactate dehydrogenase (EC 1.1.1.27) was investigated in the C6 rat glioma cell line. [3H]Leucine-labeled lactate dehydrogenase in noninduced and induced cells was quantitatively immunoprecipitated with rabbit anti-rat lactate dehydrogenase-5 antiserum. The immunoprecipitates were analyzed for 3H-labeled lactate dehydrogenase by electrophoresis on sodium dodecyl sulfate-polyacrylamide gels and isoelectrofocusing. Using this technique, it was shown that isoproterenol + 3-isobutyl-1-methylxanthine and dibutyryl cAMP cause an increase of the [3H]leucine incorporation into glioma cell lactate dehydrogenase. Analysis of the kinetics of induction and deinduction revealed no change in the rate of degradation of lactate dehydrogenase in the presence and absence of inducing agent, indicating that the induction was due to an increase in the rate of synthesis of the enzyme. The increased rate of synthesis was prevented by actinomycin D. Isoproterenol + 3-isobutyl-1-methylxanthine increased only the specific rate of synthesis of lactate dehydrogenase-5 isozyme and of the M subunit. The mechanism was further studied by assaying the level of functional mRNA coding for lactate dehydrogenase in a reticulocyte cell-free protein-synthesizing system using glioma cell poly(A)-containing RNA isolated from either isoproterenol or dibutyryl cAMP-induced cells. Analysis of the immunoprecipitated translation product by isoelectrofocusing revealed that isoproterenol or dibutyryl cAMP produced an approximately 8-fold stimulation of the poly(A) + RNA-directed synthesis of the lactate dehydrogenase M subunit. These data demonstrate that isoproterenol and dibutyryl cAMP control the level of functionally active lactate dehydrogenase mRNA in glioma cells which, in turn, determines the extent of synthesis of the lactate dehydrogenase M subunit.

1-Methyl-3-isobutylxanthine↗

PubMed2000

Effects of high and low blood lactate concentrations on sweat lactate response.

Sweat lactate results from eccrine gland metabolism, however, the possible clearance of blood lactate through sweat has not been resolved. On separate days in an environmental chamber (32 +/- 1 C) 12 subjects completed a constant load (CON) (30 min at 40% VO2 max) and an interval cycling trial (INT) (15 one-min intervals at 80% VO2 max, each separated by one min rest) each designed to elicit different blood lactate responses. Each 30 min cycling trial was preceded by 15 min warm-up (30 watts) and followed by 15 min passive rest. Sweat and blood were analyzed for lactate concentration at 15, 25, 35, 45, and 60 min during CON and INT. Total body water loss was used to calculate sweat rate (ml/hr). Blood lactate was significantly greater (p < or = 0.05) at 25, 35, 45, and 60 min during INT compared to CON (approximately 5 mmol/L vs 1.5 mmol/L). Sweat lactate was not significantly different (p>0.05) between trials at any time (approximately 10 mmol/L). Sweat rates (approximately 600ml/hr) and estimated total lactate secretion were not significantly different (CON vs. INT) (p > 0.05). Elevated blood lactate was not associated with changes in sweat lactate concentration. Sweat lactate seems to originate in eccrine glands independent of blood lactate.

Adult↗

PubMed2005

Brain lactate kinetics: Modeling evidence for neuronal lactate uptake upon activation.

A critical issue in brain energy metabolism is whether lactate produced within the brain by astrocytes is taken up and metabolized by neurons upon activation. Although there is ample evidence that neurons can efficiently use lactate as an energy substrate, at least in vitro, few experimental data exist to indicate that it is indeed the case in vivo. To address this question, we used a modeling approach to determine which mechanisms are necessary to explain typical brain lactate kinetics observed upon activation. On the basis of a previously validated model that takes into account the compartmentalization of energy metabolism, we developed a mathematical model of brain lactate kinetics, which was applied to published data describing the changes in extracellular lactate levels upon activation. Results show that the initial dip in the extracellular lactate concentration observed at the onset of stimulation can only be satisfactorily explained by a rapid uptake within an intraparenchymal cellular compartment. In contrast, neither blood flow increase, nor extracellular pH variation can be major causes of the lactate initial dip, whereas tissue lactate diffusion only tends to reduce its amplitude. The kinetic properties of monocarboxylate transporter isoforms strongly suggest that neurons represent the most likely compartment for activation-induced lactate uptake and that neuronal lactate utilization occurring early after activation onset is responsible for the initial dip in brain lactate levels observed in both animals and humans.

Animals↗