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PubMed1977

Metabolism of D- and L-lactate by Pseudomonas putida.

Pseudomonas putida grew at the same rate with the same molar growth yield on D-, L, or DL-lactate as the sole source of carbon for growth. D- and L- lactate were utilized simultaneously and at the same rate when the organism was grown on DL-lactate (ratio of D isomer to L isomer of 1:1). Growth on either isomer alone, or in combination, caused the induction of both a D-lactate, and an L-lactate dehydrogenase. Both enzymes were particulate and used dichlorophenolindophenol, or oxygen, but not NAD, as electron acceptor, and were inhibited by cyanide when oxygen was the electron acceptor. The pH optimum for the D-lactate dehydrogenase was about 6.5, and for the L-lactate dehydrogenase was about 8.0. The D-lactate dehydrogenase was more heat-sensitive than the L-lactate dehydrogenase. The stoichiometry of both enzyme reactions was the same with 2 mol of lactate dehydrogenase. The stoichiometry of both enzyme reactions was the same with 2 mol of lactate being oxidized by 1 mol of oxygen to form 2 mol of pyruvate. No lactate racemase was detected in the cell extracts.

Enzyme Induction↗
PubMed1983

Blood flow and nutrient exchange across the liver and gut of the dairy cow. Effects of lactation and fasting.

The rate of blood flow in the portal and hepatic veins, and the net exchange across the gut and liver of volatile fatty acids (VFA), glucose, lactate, pyruvate, amino acids, ketone bodies, glycerol, non-esterified fatty acids (NEFA) and oxygen, were measured in lactating and non-lactating cows (a) in the normal, fed state and (b) before, during and after 6 d of fasting. Blood flow rate through the liver was 52% higher in normal, fed, lactating cows as compared with non-lactating cows, and was decreased by fasting in both groups of cows. Portal blood flow rate increased with an increase in metabolizable energy (ME) intake. Lactating, as compared with non-lactating, cows exhibited lower arterial concentrations of glucose and lactate, higher net portal outputs of VFA and ketone bodies, a higher net hepatic output of glucose, and higher net hepatic uptake of propionate and lactate. The splanchnic outputs of acetate, glucose and hydroxybutyrate were all apparently greater in the lactating cows. Fasting caused a rapid decrease in the blood concentrations of the VFA and an increase in those of glycerol and NEFA. The portal, i.e. gut, outputs of VFA, lactate, ketone bodies, alanine and (serine + threonine), and the portal uptake of O2, were all decreased by fasting. Fasting for 6 h also decreased the hepatic output of glucose and acetate by 77 and 95% respectively, increased the hepatic uptake of pyruvate, glycerol and NEFA, and doubled hepatic ketone-body output. The splanchnic output of acetate and glucose and the splanchnic uptake of O2 were also decreased by fasting. The net portal outputs of VFA, lactate and hydroxybutyrate, and the net hepatic output of glucose, were all correlated with ME intake in fed and fasted cows. Hepatic glucose output was also correlated with milk yield. The net hepatic uptake of gluconeogenic precursors measured in this study could account for net hepatic glucose output in the fasted cows, but not in the fed cows. The net hepatic uptake of the ketogenic precursors butyrate and NEFA was sufficient to account for the hepatic output of ketone bodies in both fed and fasted cows, but it is unlikely that the hepatic uptake of ketogenic precursors could also account for the observed hepatic output of acetate.

Amino Acids↗
PubMed1995

Diversity of lactate metabolism in halophilic archaea.

D-Lactate is readily used as a substrate for the growth of species of halophilic archaea belonging to the genera Haloferax and Haloarcula. L-Lactate was used by Haloferax species (Haloferax volcanii, Haloferax mediterranei) only when a substantial concentration of the D-isomer was also present in the medium. On the enzymatic level, considerable diversity was found in the lactate metabolism of the different representatives of the Halobacteriaceae. At least three types of lactate dehydrogenases were detected in halophilic archaea. A high level of activity of an NAD-linked enzyme was present constitutively in Haloarcula species, and a low level of activity was also detected in Haloferax mediterranei. NAD-independent lactate dehydrogenases, oxidizing L-lactate and D-lactate with 2,6-dichlorophenol-indophenol as electron acceptor, were detected in all nine species tested, but L-lactate dehydrogenase activity in Halobacterium species was very low, and Haloarcula species, which possess a high level of activity of NAD-linked lactate dehydrogenase, showed very low activities of both NAD-independent D- and L-lactate dehydrogenase. An inducible lactate racemase, displaying an unusually high pH optimum, was found in Haloferax volcanii. Lactate racemase activity was found constitutively in Haloarcula species, but no activity was detected in Halobacterium species and in Haloferax mediterranei.

Halobacteriaceae↗
PubMed1999

Role of pyruvate dehydrogenase in lactate production in exercising human skeletal muscle.

The mechanisms responsible for lactate production with increased intensity of muscle contraction are controversial. Some investigators suggest that the mitochondria are O2-limited, whereas others suggest that lactate production occurs when O2 to the mitochondria is adequate and that the increased lactate production is due to a "mass-action effect" when pyruvate production exceeds the rate of pyruvate oxidation. Pyruvate dehydrogenase is a rate-limiting enzyme for pyruvate entry into the tricarboxylic acid cycle; its catalytic activity influences both pyruvate oxidation and lactate production. Since lactate dehydrogenase is an equilibrium enzyme, increased lactate production will be due to a mass-action effect exerted by increases in pyruvate concentrations. Because the equilibrium constant of the lactate dehydrogenase reaction markedly favors lactate over pyruvate, small increases in pyruvate concentration will result in large increases in lactate concentration. At higher exercise intensities, which are more reliant on glycogen as substrate, the rate of pyruvate production exceeds the catalytic activity of pyruvate dehydrogenase, and lactate production occurs. Studies using dichloroacetate, induced acid-base changes, diet and short-term endurance training, indicate that lactate production is related to complex interactions of metabolic pathways and not related to inadequate O2 supply. As pyruvate dehydrogenase plays a central role in the integration of carbohydrate and fat metabolism, and in the entry of pyruvate into the tricarboxylic acid cycle, this enzyme plays a key role in lactate production.

Exercise↗
PubMed1980

Polar distribution of sodium-dependent and sodium-independent transport system for L-lactate in the plasma membrane of rat enterocytes.

The uptake of L-lactate by rat small intestinal brush-border and basal-lateral plasma membrane vesicles has been studied. L-Lactate uptake by the isolated membrane vesicles is osmotically sensitive and represents predominantly transport into an intravesicular space and not binding to the membranes. The transport of L-lactate across the brush-border membrane is stimulated by sodium, whereas the transport across the basal-lateral plasma membrane is sodium-independent. In both types of membrane vesicles L-lactate is transported faster than D-lactate and L-lactate transport is inhibited by alpha-cyano-cinnamic acid. L-Lactate transport across basal-lateral membranes is inhibited by D-lactate and pyruvate and transstimulated by L-lactate and pyruvate. The polar distribution of transport system for L-lactate in the plasma membrane of rat enterocytes--a Na+/L-lactate cotransport system in the brush-border membrane and a facilitated diffusion system in the basal-lateral membrane--can explain the fact that in the intact epithelium L-lactate produced by cell metabolism is preferentially released on the serosal side and could enable the cell to perform vectorial, secondary active transport of L-lactate from the intestinal lumen to the serosal compartment.

Animals↗
PubMed1995

A study of lactate metabolism without tracer during passive and active postexercise recovery in humans.

Tracers have been used extensively to study lactate metabolism in humans during rest and exercise. Nevertheless, quantification of in vivo lactate kinetics as measured by lactate tracers remains controversial and new data are necessary to clarify the issue. The present study has developed a simple kinetic model which does not require labelled molecules and which yields proportional and quantitative information on lactate metabolism in humans during postexercise recovery performed at different levels of intensity. Five subjects took part in six experiments each of which began with the same strenuous exercise (StrEx; 1 min, 385 W, 110 rpm). The StrEx of each session was followed by a different intensity of recovery: passive recovery (PR) and active recoveries (AR) with power outputs of 60, 90, 120, 150 and 180 W, respectively. Blood lactate concentration was measured prior to and immediately after StrEX and regularly during the 1st h of recovery. Oxygen uptake (VO2) was measured every 30 s during the whole session. The results showed that the disappearance rate constant (ke) increases abruptly from PR [0.080 (SEM 0.004) min-1] to moderate AR [60 W: 0.189 (SEM 0.039) min-1] and decreases slowly during more intense AR [180 W: 0.125 (SEM 0.027) min-1]. The lactate apparent clearance (Cl.F-1) was calculated from the area under the lactate concentration-time curve. The Cl.F-1 increased 1.81 (SEM 0.17) fold from PR to moderate AR (60 W) and only 1.31 (SEM 0.14) from PR to the most intense AR (180 W). Using the model, the apparent lactate production (F"K0) was also calculated. The F"K0 increased regularly following a slightly curvilinear function of VO2 and was 2.61 (SEM 0.53) fold greater during the most intense AR (180 W) than during PR. Because of the lack of data concerning the size of apparent lactate distribution volume (Vd), the apparent turnover rate (Rbl) has been presented here related to Vd. The Rbl.Vd-1 increased also following a slightly curvilinear function of VO2. The Rbl.Vd-1 was 85.90 (SEM 14.42) mumol.min-1.l-1 during PR and reached 314.09 (SEM 153.95) mumol.min-1.l-1 during the most intense AR (180 W). In conclusion the model presented here does not require labelled molecules and firstly makes it possible to follow the proportional change of apparent lactate clearance and apparent lactate production during active postexercise recovery in comparison with passive recovery conditions and secondly to estimate the blood lactate turnover.

Adult↗
PubMed1985

D-lactate encephalopathy.

Although D-lactate is not a product of human intermediary metabolism, absorption of D-lactate produced by abnormal intestinal bacteria can cause systemic acidosis in patients who have undergone gastrointestinal surgery, particularly jejunoileal bypass. In order to learn more about the prevalence of D-lactate encephalopathy, its occurrence in other disorders, and how well D-lactate concentration correlates with clinical symptoms, serum D-lactate levels were determined in several specific populations. D-lactate was undetectable (less than 0.5 mmol/liter) in 72 healthy volunteers and 57 obese persons. In 33 patients who had jejunoileal bypass, 16 reported symptoms consistent with D-lactate encephalopathy since surgery. Nine of these 16 had D-lactate levels greater than 0.5 mmol/liter (range 0.7 to 11.5 mmol/liter). Levels of D-lactate fluctuated over time, and in two patients, markedly elevated levels correlated with an encephalopathy accompanied by hyperchloremic metabolic acidosis and elevated anion gap. In 470 randomly chosen hospitalized patients, D-lactate level greater than 0.5 mmol/liter was found in 13 (2.8 percent), and 60 percent of these had a history of gastrointestinal surgery or disease. It is concluded that elevated serum D-lactate levels are relatively common in patients with jejunoileal bypass, and although more rare, occur in other gastrointestinal disorders as well. The symptoms of D-lactate encephalopathy are quite sensitive, but not necessarily specific for this disorder.

Acidosis↗
PubMed1990

Central nervous system effects of lactate infusion in primates.

The concentration of total lactate in cisternal fluid increased threefold, from 12.3 +/- 2.1 to 37.6 +/- 8.9 mg/dl, during a 20-min intravenous infusion of 1 M racemic sodium lactate (10 mEq/kg) in 3 anesthetized, mechanically ventilated baboons. Rises in cisternal lactate lagged behind arterial lactate increases, but occurred during the time interval in which susceptible humans typically panic in response to lactate infusion. Subsequent to cisternal lactate increases, cisternal pH and HCO3- concentration progressively increased during a 105-min interval following lactate infusion. No consistent changes in cisternal pCO2 occurred during or subsequent to lactate infusion. These preliminary findings fail to support the hypothesis that lactate-induced panic is mediated by increasing central nervous system pCO2. Instead, these data demonstrate that lactate can rapidly increase in the central nervous system during lactate infusion, suggesting new lines of investigation for studying the mechanisms responsible for lactate-induced panic.

Animals↗
PubMed1990

Myocardial metabolism during hypoxia: maintained lactate oxidation during increased glycolysis.

In the intact animal, myocardial lactate utilization and oxidation during hypoxia are not well understood. Nine dogs were chronically instrumented with flow probes on the left anterior descending coronary artery and with a coronary sinus sampling catheter. [14C]lactate and [13C]glucose tracers, or [13C]lactate and [14C]glucose were administered to quantitate lactate and glucose oxidation, lactate conversion to glucose, and simultaneous lactate extraction and release. The animals were anesthetized and exposed to 90 minutes of severe hypoxia (PO2 = 25 +/- 4 torr). Hypoxia resulted in significant increases in heart rate, cardiac output and myocardial blood flow, but no significant change in myocardial oxygen consumption. The arterial/coronary sinus differences for glucose and lactate did not change from normoxia to hypoxia; however, the rate of glucose uptake increased significantly due to the increase in myocardial blood flow. Tracer-measured lactate extraction did not decrease with hypoxia, despite a 250% increase in lactate release. During hypoxia, 90% +/- 4% of the extracted 14C-lactate was accounted for by the appearance of 14CO2 in the coronary sinus, compared with 88% +/- 4% during normoxia. Thus, in addition to the expected increase in glucose uptake and lactate production, we observed an increase in lactate oxidation during hypoxia.

Acetates↗
PubMed1995

Influence of stage of lactation on glucose and glutamine metabolism in isolated enterocytes from dairy cattle.

Pathways of glutamine and glucose metabolism in early-, mid-, and late-lactation dairy cows were evaluated by in vitro incubations of enterocytes for 2 hours with [U-14-C]glutamine and [U-14C]glucose. Enterocytes from early-lactation cows produced greater amounts of CO2 from glutamine in concentrations that ranged from 2 to 8 mmol/L than enterocytes from either mid- or late-lactation cows. Enterocytes from early-lactation cows also produced greater amounts of CO2 from 4 and 6 mmol/L glucose than enterocytes from either mid- or late-lactation cows. Glutamine was metabolized via glutaminolysis mainly to ammonia, alanine, aspartate, glutamate, and CO2, and more of these products were produced in enterocytes from early-lactation cows than from pooled mid- and late-lactation (PML) cows. Glucose was metabolized mainly to lactate, as compared with pyruvate and CO2. Lactate and CO2 production were both greater in enterocytes from early-lactation cows than from PML cows. Glutamine as the sole substrate accounted for all the energy requirements of enterocytes from early-lactation cows but contributed only 31% in the presence of glucose. Similarly, glucose accounted for all the energy requirements of enterocytes from early-lactation cows and contributed 69% in the presence of glutamine. In enterocytes from all cows, the rate of adenosine triphosphate (ATP) production was greater in the presence of both glucose and glutamine compared with that in the presence of either substrate alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

Physiologically based pharmacokinetic modeling of the lactating rat and nursing pup: a multiroute exposure model for trichloroethylene and its metabolite, trichloroacetic acid.

A physiologically based pharmacokinetic (PB-PK) model was developed to describe trichloroethylene (TCE) kinetics in the lactating rat and nursing pup. The lactating dam was exposed to TCE either by inhalation or by ingestion in drinking water. The nursing pup's exposure to TCE was by ingestion of maternal milk containing TCE. The kinetics of trichloroacetic acid (TCA), a metabolite of TCE, were described in the lactating dam and developing pup by a hybrid one-compartment model. The lactating dam's exposure to TCA was from metabolism of TCE to TCA. The pup's exposure to TCA was from metabolism of TCE ingested in suckled milk and from direct ingestion of TCA in maternal milk. For the PB-PK model, partition coefficients (PCs) were determined by vial equilibration, and metabolic constants for TCE oxidation, by gas uptake methods. The blood/air and the fat/blood PCs for the dam were 13.1 and 34.2, and for the pup, 10.6 and 42.3, respectively. The milk/blood PC for the dam was 7.1. In lactating rats and rat pups (19-21 days old) the maximum velocities of oxidative metabolism were 9.26 +/- 0.073 and 12.94 +/- 0.107 mg/kg/hr. The plasma elimination rate constant (K = 0.063 +/- 0.004 hr-1) and apparent volume of distribution (Vd = 0.568 liter/kg) for TCA in the lactating dam were estimated from both intravenous dosing studies and an inhalation study with TCE. For the pup, K (0.014 +/- hr-1) and Vd (0.511 liter/kg) were estimated from a single 4-hr inhalation exposure with TCE. The dose-rate-dependent stoichiometric yield of TCA from oxidative metabolism of TCE in the lactating rat is 0.17 for a low-concentration inhalation exposure (27 ppm TCE) and 0.27 for an exposure above metabolic saturation (about 600 ppm TCE). For the pup, the stoichiometric yield of TCA is 0.12. With changing physiological values during lactation for compartmental volumes, blood flows, and milk yields obtained from the published literature and kinetic parameters and PCs determined by experimentation, a PB-PK model was constructed to predict maternal and pup concentrations of TCE and TCA. To test the fidelity of the PB-PK lactation model, a multiday inhalation exposure study was conducted from Days 3 to 14 of lactation and a drinking water study, from Days 3 to 21 of lactation. The inhalation exposure was 4 hr/day, 5 days/week, at 610 ppm. The TCE concentration in the drinking water was 333 micrograms/ml. Prediction compared favorably with limited data obtained at restricted time points during the period of lactation.

Animals↗
PubMed1991

Studies of the mechanism of activation of HIT-T15 cells by lactate.

L-Lactate, D-lactate, propionate and acetate (all 20 mM) caused a marked intracellular acidification in HIT-T15 cells loaded with 2'7'-bis(carboxyethyl)-5'(6')-carboxyfluorescein (BCECF), followed by recovery to more alkaline values. The effects of L- and D-lactate, but not propionate or acetate, were inhibited by 5 mM alpha-fluorocinnamate. Both L- and D-lactate caused a marked depolarisation and rise in cytosolic [Ca2+] in HIT cells as assessed by oxonol-V and quin2 fluorescence, respectively. Propionate had similar, though less marked, effects, whereas acetate exerted only a modest influence on membrane potential and cytosolic [Ca2+]. The rate of oxidation of L-lactate by HIT cells greatly exceeded that of D-lactate. alpha-Fluorocinnamate delayed, but did not prevent, the effects of L-lactate on HIT cell membrane potential or cytosolic [Ca2+]. L-lactate diminished the rate of efflux of 86Rb+ from preloaded HIT cells. Inhibition of calcium- and nucleotide-sensitive K+ channels with tetraethylammonium and tolbutamide also reduced the 86Rb+ efflux rate, and prevented any further reduction in response to L-lactate. However, such inhibition of K+ channels did not prevent a further depolarisation and rise in cytosolic [Ca2+] upon the subsequent addition of lactate. It is suggested that the activation of HIT-T15 cells by lactate is not the result of intracellular acidification or increased metabolic flux, and does not require diminished K+ permeability. An alternative mechanism is based upon the possible electrogenic flux of lactate across the plasma membrane.

Acetates↗
PubMed1988

Glutamine and ketone-body metabolism in the small intestine of starved peak-lactating rats.

1. The effect of starvation on the metabolism of gut glutamine and ketone-bodies of peak lactating, non-lactating and virgin rats was investigated. 2. The arterial blood ketone-body concentration was increased by approximately 7-, 6- and 13-fold in 48 h-starved virgin, non-lactating and lactating rats, respectively. 3. The arterial blood glutamine concentration was decreased by approximately 32% in 48 h-starved lactating rats (p less than 0.001). 4. The maximal activity of phosphate-dependent glutaminase was increased or decreased in the small intestine of fed or 48 h-starved peak-lactating rats, respectively. 5. Portal drained viscera blood flow increased by approximately 25% in peak-lactating rats. 6. Arteriovenous difference measurements for ketone-bodies across the gut of 48 h-starved rats showed an increase in net uptake of ketone-bodies by approximately 10-, 17- and 29-fold in virgin, non-lactating and lactating rats, respectively. 7. Glutamine was extracted by the gut of peak-lactating rats at a rate of 487 nmol/100 g of body wt. which was greater by approximately 33% (p less than 0.001) than that of virgin or non-lactating animals. In peak lactating rats, 48 h-starvation resulted in marked decreases in the rates of glutamine removal from the circulation (p less than 0.001) which was accompanied by decreased rates of release of glutamate, alanine and ammonia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Lactate formation by rat small intestine in vitro.

The formation of lactic acid by mucosal slices, rings and muscle from rat jejunum has been studied for periods of up to 8 min. Lactate output by mucosal slices incubated in the absence of glucose was characterised by two phases: a rapid, initial phase of release lasting about 1 min, followed by a much slower phase extending over the remainder of the incubation period. Glucose addition at 30 s initiated a second rapid phase of lactate release into the medium which was again followed by a slower rate of lactate output up to 8 min. The time course of lactate output suggested that there was a negative Pasteur effect in mucosal slices, which could not be reversed by the addition of ADP or glucose 6-phosphate. By contrast, the rate of lactate formation by rings and muscle from rat jejunum increased steadily over the incubation period, indicating a positive Pasteur effect. When Na+ in the incubating medium were replaced by K+, lactate formation by mucosal slices and rings was considerably reduced. Measurements of tissue lactate content before and during incubation revealed that about three-quarters of the lactate released by mucosal slices during the first 30 s of incubation was present initially in the tissue. After the first 30 s the tissue lactate remained constant both in the presence and absence of glucose so that the lactate released into the incubation medium is equivalent to the lactate formed by the slices. The role of the various tissue components of the small intestine in lactate formation is discussed in relation to sites of glucose entry.

Adenosine Diphosphate↗
PubMed1995

Abolition of the inhibitory effect of ethanol oxidation on gluconeogenesis from lactate by asparagine or low concentrations of ammonia.

When isolated hepatocytes from fasted rats were incubated with 10 mM lactate, the [lactate]/[pyruvate] ratio measured at the beginning of the incubation was raised above 70:1 but declined to a steady level of about 8:1 within 40 min. The rate of gluconeogenesis from lactate was initially slow but gradually increased over the incubation period becoming maximal by 30 min. The simultaneous addition of lactate and ethanol resulted in an initial [lactate]/[pyruvate] ratio above 250:1 which by 60 min had declined to a new steady-state level of approx. 60:1. The lactate, ethanol combination also brought about a prolongation of the lag phase before glucose synthesis became maximal; however, by 40 min the rate of gluconeogenesis was independent of the presence of ethanol. Thus the inhibitory effect of ethanol on glucose synthesis was manifest only over the early portion of the incubation period. When asparagine, a precursor of malate/aspartate components, was added to the incubation mixture, the lag before maximal rates of glucose formation from lactate in the absence or presence of ethanol was almost abolished. The presence of asparagine also rapidly lowered the [lactate]/[pyruvate] ratio of hepatocytes incubated with lactate plus ethanol establishing a steady-state level of 15:1 within 10-15 min. Asparagine enhanced the rate of lactate-stimulated ethanol oxidation, particularly during the early part of the incubation. In endeavouring to elucidate which of the products of asparagine catabolism (i.e. ammonia and aspartate) were responsible for these effects, we found that a small and constant level of ammonia, formed by the degradation of urea by urease, almost reproduced the effects of asparagine on the [lactate]/[pyruvate] ratio, glucose synthesis and ethanol oxidation. A bolus addition of 10 mM aspartate or 4 mM ammonia to cells metabolising lactate and ethanol were less effective than a steady-state low ammonia concentration, generated from urea/urease. Our studies suggest that asparagine or a low concentration of ammonia, by providing components of the malate/aspartate shuttle, can ameliorate some of the metabolic effects of ethanol on the liver.

Ammonia↗
PubMed1993

Changes in pituitary, hypothalamic and brain progestin-metabolizing enzyme activities during lactation.

Progesterone 5 alpha-reductase activity and 5 alpha-dihydroprogesterone 3 alpha-hydroxysteroid oxidoreductase (3 alpha-HSOR) activities (NADH- and NADPH-linked) were measured in anterior pituitaries, hypothalami and brains from lactating rats (8 and 21 days postpartum) and non-lactating (60-day-old cycling) rats. Tissue levels of these three enzyme activities varied significantly among the three groups examined. In terms of pituitary, mean levels of both of its 3 alpha-HSOR activities were 40-140% higher in actively lactating rats (8 days postpartum) relative to mean levels in lactating rats at weaning (21 days postpartum) or in non-lactating rats. There were no differences in pituitary progesterone 5 alpha-reductase activity among the three experimental groups. In the hypothalamus, the NADPH-linked 3 alpha-HSOR was elevated (50%) at 8 days of lactation compared to the group at 21 days. Hypothalamic NADH-linked 3 alpha-HSOR levels did not vary among the 3 groups. Hypothalamic progesterone 5 alpha-reductase levels in the actively lactating and weaning groups were 30% lower than those of the non-lactating group. Brain levels of progesterone 5 alpha-reductase were also lower in these two lactating groups (35-55%) as compared to the non-lactating control group. In brain, NADPH 3 alpha-HSOR activity did not vary among the three groups, but levels of NADH 3 alpha-HSOR activity were lower (40-50%) in the weaning group as compared to the actively lactating and control groups. These findings suggest the possibility that tissue changes in these progesterone-metabolizing enzyme activities during lactation and at weaning are influencing the in situ supply of 3 alpha,5 alpha-tetrahydroprogesterone and 5 alpha-dihydroprogesterone and their derivative effects on GABAA receptor activity and prolactin and gonadotropin release. The decreased activity of progesterone 5 alpha-reductase in hypothalamus and brain would presumably reduce in situ 5 alpha-dihydroprogesterone formation while increases in 3 alpha-HSOR activity would suggest higher in situ 3 alpha,5 alpha-tetrahydroprogesterone formation, especially in the pituitary.

3-Hydroxysteroid Dehydrogenases↗
PubMed2006

Discordance between lactate and base deficit in the surgical intensive care unit: which one do you trust?

PURPOSE: Both lactate and base deficit (BD) are used as predictors of injury severity and mortality. We examined the significance of these measures when used in combination, and particularly when they provide conflicting data. METHODS: We reviewed all intensive care unit patients with simultaneously obtained lactate and BD measurements. The ability to predict mortality and hospital stay was compared alone, in combination, and when there was disagreement between the measures. Receiver operating characteristic curves were generated to compare predictive abilities. RESULTS: There were 1,298 patients with 12,197 sets of paired laboratory data; 1,026 trauma patients and 272 surgical patients. Lactic acidosis was present in 41% and a significant BD level (> 2) was found in 52%. Nonsurvivors had higher admission lactate (6.2 vs. 3.3) and base deficit (6.1 vs. 3.2) levels than survivors (both P < .01), with a modest correlation (r = .52) between the measures. The admission lactate and BD levels had similar predictive ability for mortality, with areas under the receiver operating characteristic curve of .7 and .66, respectively (both P < .01). However, the predictive ability of the BD level decreased significantly during the intensive care unit stay (area, .5) compared with lactate level (area, .68). Lactate and BD levels disagreed in 44% of all laboratory sets. In patients with a normal lactate level (< 2.2), the BD level had no predictive ability for mortality (area, .48; P = .26). However, in patients with a normal BD level (< 2.0), the lactate level retained its predictive ability for mortality (area, .67; P < .01). Lengths of stay were longer among patients with an increased lactate level, even when the BD level was normal. There was no improvement in predictive ability using a combination of the 2 measures. CONCLUSIONS: Both lactate and BD levels may be used to identify lactic acidosis and predict mortality at admission. Increased lactate levels predict mortality and a prolonged course regardless of the associated BD level, whereas an increased BD level has no predictive value if the lactate level is normal.

Acid-Base Imbalance↗
PubMed2005

GH secretory responses to ghrelin and GHRH in growing and lactating dairy cattle.

Release of growth hormone (GH) is known to be regulated mainly by GH-releasing hormone (GHRH) and somatostatin (SRIF) secreted from the hypothalamus. A novel peripheral release-regulating hormone, ghrelin, was recently identified. In this study, differences of the GH secretory response to ghrelin and GHRH in growing and lactating dairy cattle were investigated and an alteration of plasma ghrelin levels was observed. The same amounts of ghrelin and GHRH (0.3 nmol/kg) were intravenously injected to suckling and weanling calves, early and mid-lactating cows and non-lactating cows. Plasma ghrelin levels were also determined in dairy cattle in various physiological conditions. The peak values of ghrelin-induced GH secretion were increased in early lactating cows compared to those in non-lactating cows. The relative responsiveness of GH secretion to ghrelin was also increased compared with that to GHRH in early lactating cows. GH secretory responses to GHRH were blunted in mature cows with and without lactation. Conversely, GHRH-induced GH secretory response was greater than that to ghrelin in calves, and also greater in calves than in mature cows. Plasma ghrelin concentrations were elevated in early lactating cows compared to those in non-lactating cows. Plasma GH concentrations were higher in suckling calves and early lactating cows compared with those in non-lactating cows. These results suggest that GHRH is an effective inducer of GH release in growing calves, and that the relative importance of ghrelin in contributing to the rise in plasma GH increases in early lactating cows.

Animals↗