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PubMed1980

Glucose and lactate metabolism in vivo in ovine fetus.

The metabolism of glucose and lactate by the ovine fetus (123-128 days of gestation) was studied; a primed, continuous infusion of [2-3H]glucose and [U-14C]lactate into the brachial vein of six fetuses was used. Fetal plasma lactate concentrations averaged 2.12 +/- 0.25 mM and glucose concentrations averaged 9.3 +/- 1.3 mg/100 ml. Total plasma turnover of lactate was 5.22 +/- 0.7 nmol/h and that of glucose was 3.48 +/- 0.63 nmol x h-1 x kg fetal weight-1. Lactate was converted to glucose at a rate of 1.35 +/- 0.64 mmol x h-1 x kg fetal weight-1, which represented 21.6 +/- 6.0% of the lactate turnover. The percentage of glucose coming from lactate was 48.9 +/- 15.2. The specific activity of maternal plasma glucose was less than 4% of the specific activity of glucose observed in fetal plasma. No radioactivity could be detected in maternal plasma lactate. The data show that the ovine fetus or the fetal-placental unit can convert lactate to glucose by days 123-128 of gestation. A general model presented describes carbohydrate metabolism in the ovine placenta and fetus.

Animals↗

PubMed1987

Sympathetic activity in brown adipose tissue in lactating mice.

Sympathetic activity has been assessed, by measurements of norepinephrine turnover, in interscapular brown adipose tissue of mice during lactation. Norepinephrine turnover was reduced in brown adipose tissue from early lactation until weaning. The reduction in turnover occurred in dams suckling either large-or small-sized litters. Norepinephrine turnover returned to the control level after natural weaning and increased rapidly after abrupt weaning at peak lactation. Acute exposure to cold resulted in a large increase in norepinephrine turnover in brown adipose tissue of lactating mice, as in control animals. These results indicate that sympathetic activity is suppressed in brown adipose tissue during lactation, but sympathetic responsiveness is retained. The reduction in sympathetic activity is likely to be responsible for the decrease in brown adipose tissue thermogenesis in lactation. Norepinephrine turnover in the heart tended to be reduced at peak lactation, suggesting that there may be a general decrease in sympathetic activity in the lactating animal. In contrast to the normal animal, the hyperphagia of lactation does not lead to an activation of the sympathetic nervous system.

Adipose Tissue, Brown↗

PubMed1992

Bone mineral loss during lactation occurs in absence of parathyroid tissue.

The requirement of parathyroid tissue for bone mineral loss during lactation was investigated. Lactating rats parathyroidectomized (PTX) at day 2 of lactation and consuming a 2% calcium diet are hypercalcemic and hypophosphatemic at day 13 of lactation. The high-calcium diet supports normal growth of pups nursing PTX mothers. PTX lactating rats mobilize bone mineral to the same extent as euparathyroid lactating rats consuming the same diet. Non-lactating PTX rats lose no bone mineral over a similar time period, indicating lactation-specific bone mineral mobilization in the absence of parathyroid tissue. PTX rats were verified to have physiologically insignificant amounts of parathyroid tissue, as evidenced by severe hypocalcemia and/or death in each rat after a shift from a 2% calcium to a 0.02% calcium diet. These results conclusively demonstrate that lactation-associated bone mineral mobilization does not require parathyroid hormone or parathyroid tissue.

Animals↗

PubMed1994

Lactate-pyruvate interconversion in blood: implications for in vivo tracer studies.

We have evaluated lactate and pyruvate kinetics in whole blood or plasma by the addition of [1-13C]lactate (n = 5) or [1-13C]pyruvate (n = 5) and application of compartmental modeling to the resulting data. Pyruvate and lactate concentrations and tracer-to-tracee ratios were measured at frequent intervals for 45 min. Pyruvate and lactate tracer-to-tracee ratios equilibrated almost completely within 3-4 min in whole blood, whereas there was no isotopic exchange in plasma. The average rate of interconversion between unlabeled lactate and pyruvate was four to five times (pyruvate to lactate) and three to four times (lactate to pyruvate) the net production rate of lactate. We conclude that there is a very rapid interconversion between lactate and pyruvate in blood that has to be considered in the interpretation of in vivo tracer studies.

Adult↗

PubMed1994

Measurement of pyruvate and lactate kinetics across the hindlimb and gut of anesthetized dogs.

We have developed a new model to quantify regional pyruvate and lactate transmembrane transport, shunting, exchange, production, and oxidation in vivo. The method is based on the systemic continuous infusion of pyruvate or lactate stable isotopic carbon tracers and the measurement of pyruvate and lactate enrichment and concentration in the artery and vein of that region (e.g., leg or gut), the pyruvate and lactate enrichment of intracellular free water in the tissue as measured by biopsy, and the rate of blood flow through the tissue. The purpose of the experiment was to measure the pyruvate and lactate kinetics in leg muscle and gut in anesthetized dogs (n = 6). The transmembrane transport and degree of shunting of pyruvate and lactate were comparable in muscle and gut. When modified for substrate inflow, interconversion between pyruvate and lactate took place at a rate twice as fast in muscle as in the gut, and production and oxidation of pyruvate was approximately 50% greater in muscle than in the gut. Thus our new model enables quantitation of many aspects of lactate and pyruvate kinetics. We conclude that in anesthetized animals the muscle is the tissue most responsible for whole body peripheral pyruvate and lactate kinetics.

Anesthesia↗

PubMed1995

Stable isotope determination of plasma lactate conversion into glucose in fasting infants.

To quantify lactate gluconeogenesis, we developed a gas chromatography-mass spectrometry method based on the infusion of [6,6-2H2]glucose and [3-13C]lactate tracers to 12 infants aged 1-25 mo fasting for 11.5 +/- 1.5 h. Both rates of appearance of plasma glucose (26.7 +/- 2.6 mumol.kg-1.min-1, 4.8 +/- 0.5 mg.kg-1.min-1) and lactate (30.8 +/- 3.1 mumol.kg-1.min-1, 2.8 +/- 0.3 mg.kg-1.min-1) were remarkably elevated compared with adult values. The interconversion of plasma lactate and glucose was determined by 1) measuring the incorporation of 13C from [3-13C]lactate into plasma glucose; 2) correcting for the metabolic exchange of carbon atoms in the tricarboxylic acid cycle. For this purpose, an additional group of six infants was infused with [3-13C]lactate, and the distribution of 13C at specific carbon positions in the glucose molecule was determined using relevant ions in the electron-impact mass spectrum of its 1,2,5,6-diisopropylidene-3-O-acetyl-alpha-furanosyl derivative; and 3) measuring the reverse conversion of glucose to lactate in five other infants infused with [1-13C]glucose. We found that 54 +/- 2% of glucose was derived from plasma lactate (14.4 +/- 1.3 mumol.kg-1.min-1, 2.6 +/- 0.2 mg.kg-1.min-1). Lactate and glucose rates of appearance were correlated (r = 0.58, P < 0.05) and decreased with fasting duration (r = 0.66, P < 0.02). The correction factor for carbon exchange in the tricarboxylic acid cycle was 1.14 +/- 0.11.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗

PubMed1995

Distinguishable substrate pools for muscle glyconeogenesis in lactate-supplemented recovery from exercise.

The formation of muscle glycogen from substrates other than glucose (glyconeogenesis) has now been demonstrated 1) from circulating lactate when this lactate is elevated and 2) from intramuscular substrate, which equilibrates with the products of local glucose metabolism but not with circulating lactate [Am. J. Physiol. 267 (Endocrinol. Metab. 30): E210-E218, 1994]. The purpose of the present studies was to examine the interaction of recovery from low-intensity exercise (4-h swim) and supplementation with exogenous lactate in determining the distribution of carbon flux between these two pathways for the glyconeogenic process in the gastrocnemius muscles. Ten protocols were defined using [14C]bicarbonate (no local incorporation into glycogen), [U-14C]lactate (tracks circulating lactate), and recycled [1-14C]glucose (tracks local substrate formation and glyconeogenesis). During recovery, lactate was infused to increase circulating concentrations 15- to 20-fold. Glucose and saline infusions during recovery were used as controls. The results indicate that prior exercise primarily promotes the local incorporation of recycled glucose label produced within the muscle into glycogen. Exogenous lactate stimulates the incorporation of circulating lactate into muscle glycogen. The contribution of the two substrate pools to glycogen synthesis appears to be additive, indicating the independence of muscle glycogenesis from these two sources.

Animals↗

PubMed1996

Alterations of plasma lactate and glucose metabolism in obese children.

Using a double stable isotope infusion method, we quantified plasma glucose and lactate inter-relationships in five recently obese children. Compared with five age-matched controls, obese children had an approximately 50% increase of total body lactate turnover [167 +/- 20 vs. 111 +/- 20 (SE) mg/min, P < 0.05]. The rate of lactate conversion to glucose was double the normal rate (96 +/- 21 vs. 46 +/- 10 mg/min, P < 0.05). Increased gluconeogenesis from plasma lactate correlated with total glucose production (r = 0.74), with plasma lactate contributing to 58% of glucose production in obese children vs. 38% in normal children (P < 0.05). Conversion into glucose correlated with the rate of lactate release in the circulation (r = 0.76). In turn, the obese children converted a larger fraction (35 +/- 2 vs. 27 +/- 2%, P < 0.02) and amount (58 +/- 10 vs. 34 +/- 5 mg/min, P < 0.05) of glucose into plasma lactate. The amount of lactate originating from plasma glucose correlated (r = 0.70) with lipid oxidation, which was increased in the obese children (58 +/- 4 vs. 23 +/- 5 mg/min, P < 0.02). Our data suggest that increased gluconeogenesis from lactate is associated with increased lipid oxidation and could contribute to the progressive development of insulin resistance and glucose intolerance in juvenile obesity.

3-Hydroxybutyric Acid↗

PubMed2000

Uptake of lactate by the liver: effect of red blood cell carriage.

Multiple-indicator dilution experiments with labeled lactate were performed in the livers of anesthetized dogs. A mixture of (51)Cr-labeled erythrocytes, [(3)H]sucrose, and L-[1-(14)C]lactate or a mixture of (51)Cr-labeled erythrocytes, [(14)C]sucrose, and L-[2-(3)H]lactate was injected into the portal vein, and samples were obtained from the hepatic vein. Data were evaluated using a model comprising flow along sinusoids, exchange of lactate between plasma and erythrocytes and between plasma and hepatocytes, and, in the case of L-[1-(14)C]lactate, metabolism to H[(14)C]O(-)(3) within hepatocytes. The coefficient for lactate efflux from erythrocytes was 0.62 +/- 0.24 s(-1), and those for influx into and efflux from hepatocytes were 0.44 +/- 0.13 and 0.14 +/- 0.07 s(-1), respectively. The influx permeability-surface area product of the hepatocyte membrane for lactate (P(in)S, in ml x s(-1) x g(-1)) varied with total flow rate (F, in ml s(-1) x g(-1)) according to P(in)S = (3.1 +/- 0.5)F + (0.021 +/- 0.014). Lactate in plasma, erythrocytes, and hepatocytes was close to equilibrium, whereas lactate metabolism was rate limiting.

Acetates↗

PubMed1975

Effect of lactate infusion on myocardial FFA metabolism in diabetic dogs.

The effect of elevated arterial lactate concentration on myocardial free fatty acid (FAA), acetoacetate (AcAc), and beta-hydroxybutyrate (beta-OHB) uptake was studied in alloxan-diabetic dogs under control conditions and following the constant infusion of Na-L-(+)-lactate. Only minor changes in hemodynamic parameters were observed. During lactate infusion, arterial lactate increased and FFA, AcAc, and beta-OHB decreased. The extraction ratio and myocardial uptake of both AcAc and beta-OHB diminished. No significant change of myocardial FFA oxidation was noted. While myocardial lactate uptake was very small under control conditions, it increased considerably during the infusion of lactate. The fraction of myocardial CO2 production derived from FFA oxidation was unchanged during lactate infusion, while the fraction derived from ketone bodies decreased and that derived from lactate increased. Thus, during hyperlactacidemia a larger fraction of myocardial substrate was derived from lactate and a smaller fraction from ketone bodies than were derived under control conditions.

Acetoacetates↗

PubMed1976

Lactate production in isolated perfused rat lung.

The ability of the isolated perfused rat lung to produce lactate under aerobic and hypoxic conditions has been studied. The lung has been found capable of producing lactate at a rate of 53 mumol/g dry wt per h in the presence of as great as 1 mM extracellular lactate under aerobic conditions. Essentially 100% of the lactate synthesized was derived from [U-14C]glucose. When hypoxic, the rate of lactate production doubled, but only 60% was found to be derived from [U-14C]glucose. When the perfused lung was exposed to aerobic conditions following hypoxia, it was found that lactate production did not decrease. However, lactate production from [U-14C]glucose did increase. It is concluded that lung tissue possesses a high rate of lactate production under aerobic contitions from glucose in comparison to glucose oxidation to CO2. When the lung is hypoxic, lactate production increases as a probable result of amino acid catabolism with little anaerobic energy production occurring. The effect of hypoxia was not reversed within the duration of the performed experiments.

Animals↗

PubMed1985

Glucose and lactate kinetics in American eel Anguilla rostrata.

Simultaneous infusion of [6-3H]glucose and [U-14C]lactate was used to calculate the turnover rate of glucose, the irreversible replacement rate of lactate, and the rates of the exchange of carbon atoms between glucose and lactate in free-swimming American eels (Anguilla rostrata) fed or food deprived for 6, 15, and 36 (maturing) mo. The mean turnover rate of glucose in fed animals averaged 1.0 mg X min-1 X 100 g-1, while the lactate irreversible replacement rate was approximately 4.0 micrograms X min-1 X 100 g-1. The conversion of 35% of lactate carbon to glucose implied a substantial Cori cycle activity, but this amounted to less than 1% of total glucose production. Food deprivation for 6 mo altered few kinetic patterns, except for an increased lactate irreversible replacement rate and a minor increase in gluconeogenesis from lactate. After a 15-mo fast, glucose turnover decreased to 0.09 +/- 0.02 mg X min-1 X 100 g-1. Plasma lactate concentrations and production rates continuously increased during the experiment. Maturing eels that had been food deprived for 36 mo maintained glucose and lactate concentrations and kinetics similar to values in animals food deprived for only 6 mo. This study stresses the importance of carbohydrate in the metabolism of this species under fed and food-deprived conditions and further supports the tolerance of Anguillid species to food deprivation.

Anguilla↗

PubMed1990

Glycogenesis from lactate in rabbit skeletal muscle fiber types.

The path of glycogen synthesis from three-carbon precursors was studied via single-pass perfusions in three distinct rabbit skeletal muscle preparations, i.e., glycolytic (greater than 99% type IIb), oxidative (greater than 97% type I), and mixed (type I, IIa, and IIb). The extent of interaction between the Krebs cycle and glycogenesis was assessed utilizing [1-14C]- or [2-14C]lactate at basal (1.1 +/- 0.1 mM) and elevated (8.1 +/- 0.3 mM) lactate concentrations (protocols 1 and 2). Under conditions in which the net balance of glucose and lactate, [14C]lactate removal, and venous lactate-specific activity were similar, the yields of 14CO2 and [14C]glycogen were not significantly influenced by position of the label. Additional perfusions were performed with lactate (8.0 +/- 0.1 mM) and acetate (1.0 +/- 0.1 mM) as sole substrates and either [U-14C]lactate or [2-14C]acetate as the tracer. Under conditions of net glycogen synthesis, the incorporation of [14C]lactate into glycogen [in disintegrations/min (dpm).g-1.2 h-1] was 40,940 +/- 3,320, 1,540 +/- 320, and 32,600 +/- 4,100 in the glycolytic, oxidative, and mixed preparations, respectively. However, no incorporation of [2-14C]acetate into glycogen was observed in any preparation, despite a significant yield of 14CO2. Mercaptopicolinic acid, a potent inhibitor of phosphoenolpyruvate carboxykinase (PEPCK), demonstrated no significant effect on net substrate balance, tracer uptake, net glycogen synthesis, incorporation of [14C]lactate and [3H]-glucose into glycogen, or 14CO2 yield. Current results suggest an extramitochondrial route for net glycogen synthesis from three-carbon precursors, exclusive of PEPCK, that is consistent across all mammalian skeletal muscle fiber types.

Acetates↗

PubMed1993

Lactate and glucose metabolism in mouse (Mus musculus) and reptile (Anolis carolinensis) skeletal muscle.

The reliance on anaerobic metabolism during exercise in lizards has been the subject of a growing body of literature in activity metabolism. Prior studies have demonstrated that lizards rely more on postexercise lactate to regenerate depleted glycogen stores than do many mammals. These studies prompted an in vitro comparison between the metabolic mechanisms for the handling of lactate and glucose in the muscles of a small mammal and lizard. Hindlimb muscles of Mus and Anolis were stimulated to fatigue and then incubated in the presence of 15 mM lactate and either 5.5 (mice) or 8.5 (anoles) mM glucose. Oxidation rates of lactate and glucose were seven to eight times higher in mice. Both species oxidized more lactate than glucose (8 to 9 times). However, anole muscle showed a preference for lactate as a substrate for glycogenesis, incorporating 1.5 times as much lactate (expressed in glucose equivalents) as glucose. In contradistinction, mice incorporated 2.8 times as much glucose into glycogen as lactate. The quantitative differences in metabolic scope of mammals and reptiles are accompanied by fundamental differences in the capacity and patterns of skeletal muscle metabolism of lactate and glucose.

Animals↗

PubMed1993

Plasma catecholamine and corticosterone and their in vitro effects on lizard skeletal muscle lactate metabolism.

Lizard skeletal muscles utilize primarily lactate as a gluconeogenic substrate for glycogen replenishment following exercise. To understand the influence of selected hormones on this process, we measured changes in plasma catecholamines and corticosterone resulting from exercise in the lizard Dipsosaurus dorsalis and then investigated the physiological effects of those hormones on skeletal muscle lactate and glucose metabolism in vitro. Plasma epinephrine (Epi), norepinephrine, and corticosterone (Cort) increased 5.8, 10.2, and 2.2 times, respectively, after 5 min of exhaustive exercise. Epi and Cort levels remained elevated after 2 h of recovery. Skeletal muscle fiber bundles isolated from the red and white regions of the iliofibularis muscle were incubated 2 h at 40 degrees C in the presence of postexercise concentrations of [14C]lactate (15 mM) and glucose (8.5 mM) in the presence and absence of Epi or Cort. Red muscle oxidized both substrates at 2-3 times the rate of white muscle, and both red and white fibers oxidized lactate at 5-10 times the rate of glucose oxidation. Epi had a stimulatory effect on lactate oxidation by white muscle. Lactate incorporation into glycogen proceeded at 2-3 times the rate of glucose incorporation in both muscle types, with rates in red muscle again 2-3 times that for white muscle. Epi stimulated lactate carbon incorporation into glycogen by 50-140% in both red and white muscle but had no effect on glucose incorporation into glycogen in either tissue. We interpret these data as evidence that epinephrine stimulates lactate removal by skeletal muscle. Cort had no effect on lactate metabolism in either muscle type.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Basolateral transport of lactate in dog thick ascending limbs.

Basolateral membrane vesicles (BLMV) isolated from both red outer medulla or from thick ascending limb segments isolated from the dog kidney were used to examine the process of lactate transport in this nephron segment. The BLMV preparation was enriched in Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) that represented 96% of the total ATPase activity of this preparation and the vesicles were largely under the right side-out orientation. On application of a OH- or HCO3- gradient (inside greater than outside), a secondary active lactate accumulation was observed, with characteristic transient overshoot. This phenomenon was shown to occur irrespective of the presence or absence of Na+, K+, or Cl-. The pH, but not the bicarbonate-driven, overshoot was abolished by nigericin (in presence of K+). Studies with valinomycin and K+ demonstrated that the generation of a membrane potential was not responsible for the acceleration of lactate transport, even if the amplitude of lactate accumulation was reduced in the presence of a bicarbonate gradient and valinomycin. A significant trans-stimulation of [14C]lactate transport by cold lactate was observed (under voltage-clamp condition). The transport was 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid insensitive but sensitive to furosemide (IC50 = 0.1 mM) and alpha-hydroxycyanocinnamate (IC50 = 1 mM). The kinetic parameters of the transporter revealed a single carrier with an apparent Michaelis constant of 1.7 mM and an apparent Vmax of 9.7 nmol.mg protein-1.30 s-1. The transporter was shown to be distinct from that of proximal tubule brush-border membrane or mitochondria (pyruvate). Thus thick ascending limbs possess a carrier-mediated lactate transport that can be used for lactate uptake (aerobic condition) or for lactate release (anaerobic glycolysis) according to metabolic processes imposed by the local oxygenation condition.

Animals↗

PubMed1986

Lactate efflux is unrelated to intracellular PO2 in a working red muscle in situ.

Blood flow, lactate extraction, and tissue lactate concentration were measured in an autoperfused pure red muscle (dog gracilis). Muscles were frozen in situ during steady-twitch contraction at frequencies of 1-8 Hz [10-100% of maximum O2 consumption (VO2max)]. Myoglobin saturation was determined spectrophotometrically with subcellular spatial resolution. Intracellular PO2 (Pto2) was calculated from the oxymyoglobin-dissociation curve. Tissue lactate was well correlated with VO2 but not with Pto2. Lactate efflux increased markedly above a threshold work rate near 50% VO2max. Efflux was neither linearly correlated with tissue lactate nor related to Pto2. Pto2 exceeded the minimum PO2 for maximal VO2 in each of 2,000 cells examined in muscles frozen at 1-6 Hz. A small population of anoxic cells was found in three muscles at 8 Hz, but lactate efflux from these muscles was not greater than from six other muscles at 8 Hz. Our conclusions are that 1) the concept of an anaerobic threshold does not apply to red muscle and 2) in absence of anoxia neither tissue lactate nor blood lactate can be used to impute muscle O2 availability or glycolytic rate. A mechanism by which the blood-tissue lactate gradient could support aerobic metabolism is discussed.

Animals↗

PubMed1989

Decreased exercise muscle lactate release after high altitude acclimatization.

Blood lactate concentration during exercise decreases after acclimatization to high altitude, but it is not clear whether there is decreased lactate release from the exercising muscle or if other mechanisms are involved. We measured iliac venous and femoral arterial lactate concentrations and iliac venous blood flow during cycle exercise before and after acclimatization to 4,300 m. During hypoxia, at a given O2 consumption the venous and arterial lactate concentrations, the venous and arterial concentration differences, and the net lactate release were lower after acclimatization than during acute altitude exposure. While breathing O2-enriched air after acclimatization at a given O2 consumption the venous and arterial lactate concentrations and the venous and arterial concentration differences were significantly lower, and the net lactate release tended to be lower than while breathing ambient air at sea level before acclimatization. We conclude that the lower lactate concentration in venous and arterial blood during exercise after altitude acclimatization reflected less net release of lactate by the exercising muscles, and that this likely resulted from the acclimatization process itself rather than the hypoxia per se.

Acclimatization↗