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PubMed2001

Low bone mineral density in the femoral neck of medieval women: a result of multiparity?

An archaeological investigation of a medieval cemetery gave us the opportunity to investigate 49 Danish skeletons dating from 1000 to 1250 A.D. and to compare them with 298 contemporary Danes (aged 19-79 years) and assess the millennial trend in bone mineral density (BMD) in populations considered genetically closely related. BMD and bone mineral apparent density (BMAD) of the femoral neck were measured by dual-energy X-ray absorptiometry (DEXA) and transformed into z scores. BMD(zscore) was significantly lower in medieval women (-0.54 +/- 0.25, p = 0.04), whereas BMD(zscore) in medieval men was significantly higher (0.55 +/- 0.22, p = 0.02). In medieval women, BMD(zscore) tended to increase with age (r = 0.42, p = 0.07), whereas no change was seen in men (r = 0.19, not significant [n.s.]). Also, BMAD(zscore) was significantly elevated in medieval men (1.00 +/- 0.28, p < 0.01), but in medieval women no difference was found (-0.28 +/- 0.21, n.s.). However, the correlation between BMAD(zscore) and age was significant in the medieval women where it increased with advancing age (r = 0.49, p = 0.03). In conclusion, medieval women had lower BMD when compared with contemporary women, but this relationship was reversed in women who survived to older ages. In contrast, medieval men had significantly higher BMD as compared with contemporary men at all ages. The observed lower BMD in medieval women can be explained by the well-known selective mortality among the younger women. A high birth rate and prolonged periods of lactation are the main reasons for the observed increased mortality, and therefore can also very likely explain the associated low BMD. The increase in the incidence of osteoporosis in modern elderly women could possibly, or partially, be explained by the survival of women who would have died prematurely had they lived in earlier centuries.

Bone Density↗
PubMed1985

Circulatory shock following intravenous propoxyphene poisoning. An experimental study of cardiac function and metabolism in pentobarbital-anesthetized pigs.

The effects of continuously administered intravenous propoxyphene chloride (15 mg X min-1) on ECG, systemic, pulmonary and coronary circulations and myocardial oxygenation were investigated in eight pentobarbital-anesthetized pigs. Circulatory shock, defined as a systolic blood pressure below 60 mmHg (8.0 kPa) and a cardiac output of approximately 2.0 l X min-1 X m-2, occurred after 675 to 2025 mg propoxyphene chloride. At the time when shock occurred plasma concentrations of propoxyphene ranged from 9.6 to 15.3 micrograms X ml-1 which is within the range of the lethal concentration observed in man. Statistically significant decreases were observed for the following variables: maximum rate of rise of left ventricular pressure dP/dt (-90%), mean arterial pressure (-73%), heart rate (-46%), cardiac index (-58%), stroke volume index (-22%), left ventricular stroke work index (-85%), right ventricular stroke work index (-63%) and systemic vascular resistance (-50%). Mean pulmonary arteriolar occlusion pressure increased (+42%), whereas mean right atrial pressure and pulmonary vascular resistance remained unchanged. The arteriovenous oxygen difference increased (+53%) and total body oxygen consumption decreased (-35%). The following coronary variables decreased: coronary sinus blood flow (-57%), coronary vascular resistance (-65%), myocardial oxygen consumption (-68%), myocardial oxygen extraction (-26%) and myocardial lactate extraction (-28%). Prolongation of the ECG PQ and QRS intervals were recorded shortly before shock appeared, and all animals were in sinus rhythm till the last minute before death. The results indicate that intravenously administered propoxyphene besides being a powerful negative inotropic and chronotropic agent, is also a potent systemic and coronary vasodilator.

Anesthesia, General↗
PubMed2006

Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus.

Neurons, including their synapses, are generally ensheathed by fine processes of astrocytes, but this glial coverage can be altered under different physiological conditions that modify neuronal activity. Changes in synaptic connectivity accompany astrocytic transformations so that an increased number of synapses are associated with reduced astrocytic coverage of postsynaptic elements, whereas synaptic numbers are reduced on reestablishment of glial coverage. A system that exemplifies activity-dependent structural synaptic plasticity in the adult brain is the hypothalamo-neurohypophysial system, and in particular, its oxytocin component. Under strong, prolonged activation (parturition, lactation, chronic dehydration), extensive portions of somatic and dendritic surfaces of magnocellular oxytocin neurons are freed of intervening astrocytic processes and become directly juxtaposed. Concurrently, they are contacted by an increased number of inhibitory and excitatory synapses. Once stimulation is over, astrocytic processes again cover oxytocinergic surfaces and synaptic numbers return to baseline levels. Such observations indicate that glial ensheathment of neurons is of consequence to neuronal function, not only directly, for example by modifying synaptic transmission, but indirectly as well, by preparing neuronal surfaces for synapse turnover.

Animals↗
PubMed1995

Increased clearance of lactate after short-term training in men.

A short-term training model previously shown to result in a tighter metabolic control in working muscle in the absence of an increase in mitochondrial potential was used to examine changes in lactate turnover. Lactate flux was studied before and after 10 days of cycle training [2 h/day at 59% maximal oxygen consumption (VO2max)] in untrained men [VO2max = 45.5 +/- 2.4 (SE) ml.kg-1.min-1). A primed constant infusion of L-[1-13C]lactate was used to examine lactate kinetics during a prolonged exercise protocol (90 min at 59% VO2max). Rate of appearance of lactate increased with exercise (P < 0.01), both pretraining (rest = 30.3 +/- 4.9 ml.kg-1.min-1, exercise = 115 +/- 14 ml.kg-1.min-1) and posttraining (rest = 28.4 +/- 4.7 ml.kg-1.min-1, exercise = 112 +/- 13 ml.kg-1.min-1). Despite a lower blood lactate concentration (P < 0.05) during exercise after training, there was no difference in the rate of appearance of lactate. Training increased (P < 0.05) the metabolic clearance rate of lactate during exercise from 36.8 +/- 4.8 to 51.4 +/- 6.8 ml.kg-1.min-1. These findings indicate that at least part of the lower exercising blood lactate observed after training is due to an increase in metabolic clearance rate. In addition, the lower intramuscular lactate levels suggest a decreased recruitment of glycolysis particularly early in exercise.

Adenosine Triphosphate↗
PubMed1989

The effect of diazepam on neonatal seizure: in vivo 31P and 1H NMR study.

It is assumed that when anticonvulsants arrest seizure, there is rapid return of brain high energy phosphates and brain lactate to control values. To test this hypothesis, diazepam was administered to neonatal dogs during flurothyl-induced seizure. In vivo 31P nuclear magnetic resonance spectroscopy disclosed that diazepam quickly arrested electrographic seizure and restored brain phosphocreatine and inorganic phosphate to baseline values. In contrast, in vivo 1H nuclear magnetic resonance spectroscopic measurements showed that arrest of seizure with diazepam did not return brain lactate to control values. The sustained increase in cerebral blood flow and prolonged elevation of brain lactate, acetate, valine, and succinate in the postictal period indicate that metabolic recovery of the brain occurs over an extended period of time after the normalization of EEG, phosphocreatine, and brain pH.

Acetates↗
PubMed2007

Improving the thermal stability of lactate oxidase by directed evolution.

Lactate oxidase is used in biosensors to measure the concentration of lactate in the blood and other body fluids. Increasing the thermostability of lactate oxidase can significantly prolong the lifetime of these biosensors. We have previously obtained a variant of lactate oxidase from Aerococcus viridans with two mutations (E160G/V198I) that is significantly more thermostable than the wild-type enzyme. Here we have attempted to further improve the thermostability of E160G/V198I lactate oxidase using directed evolution. We made a mutant lactate oxidase gene library by applying error-prone PCR and DNA shuffling, and screened for thermostable mutant lactate oxidase using a plate-based assay. After three rounds of screening we obtained a thermostable mutant lactate oxidase, which has six mutations (E160G/V198I/G36S/T103S/A232S/F277Y). The half-life of this lactate oxidase at 70 degrees C was about 2 times that of E160G/V198I and about 36 times that of the wild-type enzyme. The amino acid mutation process suggests that the combined neutral mutations are important in protein evolution.

Amino Acid Substitution↗
PubMed1994

Preliminary application of magnetic resonance spectroscopy to investigate lactate-induced panic.

OBJECTIVE: To characterize changes associated with lactate-induced panic, proton magnetic resonance spectroscopy (MRS) was used to measure brain lactate during intravenous infusion of 0.5-M sodium lactate in panic disorder patients and comparison subjects. METHOD: Eight panic disorder subjects, five medicated and three unmedicated, and eight healthy comparison subjects were studied at baseline, during lactate infusion (5 meq/kg over 20 minutes), and after infusion. Localized proton MRS was used to acquire averaged spectra every 5 minutes from a 27-ml sampling volume in the insular cortex and adjacent regions. Brain lactate levels, quantitatively estimated in relationship to N-acetyl aspartate, were compared to blood lactate levels. RESULTS: The procedure was generally well tolerated; one panic subject requested early termination before lactate infusion. Significant rises in brain lactate levels occurred for all subjects during infusion. The panic patients who responded to lactate (N = 3) had significantly higher brain lactate levels before, during, and after infusion than did the comparison subjects (N = 8) and medicated patients who were lactate nonresponders (N = 4). After infusion the panic patients with lactate-induced panic exhibited a striking dissociation between decreasing blood lactate and further increases in brain lactate levels. CONCLUSIONS: These preliminary observations indicate that brain lactate increases during a standard lactate infusion. Lactate-induced panic is associated with greater increases than in comparison subjects and with prolonged elevations in brain lactate that are decoupled from falling blood lactate levels after completion of lactate infusion. Further investigation is necessary to clarify the mechanism(s) responsible for these findings and establish whether a causal relationship to the occurrence of lactate-induced panic exists.

Adult↗
PubMed1996

Cerebrospinal fluid/serum lactic acid in Nigerian children with febrile convulsions.

Cerebrospinal fluid (CSF) and serum lactic acid levels were prospectively assayed in 42 children less than 5 years old with febrile convulsions who were divided into two groups for analytical purposes, irrespective of aetiology of pyrexia. One group (24 children) had brief febrile seizures and the remaining 18 children had prolonged febrile seizures. CSF and serum lactic acid values were obtained for brief and prolonged seizures. On admission, the mean CSF lactic acid was significantly higher (p < 0.05) in children with prolonged than with brief seizures, but the mean serum lactic acid was not significantly different between the two groups. Twelve of the 18 children (67%) with prolonged seizures and elevated CSF lactate had seizure recurrence. There were no recurrences of seizures in children with a brief initial seizure and low CSF lactate. CSF lactic acid is elevated in children with prolonged seizures and this may be useful in detecting those with a prolonged seizure where the history of the duration of the seizure is not clear. Prolonged seizure has been associated with the risk of recurrence and therefore such children with elevated CSF lactic acid levels might benefit from long-term anticonvulsant therapy.

Anticonvulsants↗
PubMedDate not supplied

Effect of lactate on the recovery of CHO-KI cells from gamma radiation damage.

The effect of pre-exposure of CHO-KI cells to lactate on their capacity to recover from or repair radiation damage was examined. Prolonged pre-exposure to lactate and a number of inhibitors of glycolysis has previously been shown to reduce the cell survival after irradiation. Following a split dose of irradiation, cells pre-treated with lactate for 18 hours had a higher relative recovery factor than controls even though survival following a single dose was reduced. Where lactate was added just before irradiation it had a radiation protective effect on the single dose survival curve and no effect on recovery. To investigate a possible involvement of NADH generation via lactate dehydrogenase in the mechanism, oxamate, a non-metabolisable analogue of lactate, was investigated. It reduced the survival of irradiated CHO-KI cells following prolonged and short pre-exposure and did not significantly affect the recovery factor. It is suggested that since lactate and oxamate both inhibit glucose breakdown, their radiobiologic effects may be due to depletion of cellular energy substrates necessary for repair. In contrast, the increased recovery and short term radiation protective effect seen with lactate only may involve LDH activity.

Animals↗
PubMed1992

Cerebral lactate turnover after electroshock: in vivo measurements by 1H/13C magnetic resonance spectroscopy.

We reported earlier that brain activation by 10 s of cortical electroshock caused prolonged elevation of brain lactate without significant change in intracellular pH, brain high-energy phosphorylated metabolites, or blood gases. The metabolic state of the elevated lactate has been investigated in further experiments using combined, in vivo 1H-observed 13C-edited nuclear magnetic resonance spectroscopy (NMRS), homonuclear J-edited 1H-NMRS, and high-resolution 1H-NMRS of perchloric acid extracts to monitor concentrations and 13C-isotopic fractions of brain and blood lactate and glucose. We now report that electroshock-elevated lactate pool in rabbit brain approaches equilibrium with blood glucose within 1 h. There was nearly complete turnover of the raised lactate pool in brain; any pool of metabolically inactive lactate could not have been > 5% of the total. In the same experiments, blood lactate underwent < 50% turnover in 1 h. The new 1H-spectroscopic methods used for these experiments are readily adaptable for the study of human brain and may be useful in characterizing the metabolic state of elevated lactate pools associated with epilepsy, stroke, trauma, tumors, and other pathological conditions.

Animals↗
PubMed1991

Diaphragmatic energetics during prolonged exhaustive exercise.

The present study was carried out to examine diaphragmatic O2 extraction and lactate and ammonia production during prolonged exhaustive exercise. Experiments were performed on nine healthy exercise-conditioned ponies in which catheters had been implanted in the phrenic vein previously. Blood-gas variables and lactate and ammonia concentrations were determined on simultaneously obtained arterial and phrenic-venous blood samples at rest and during 30 min of exertion at 15 mph + 7% grade (heart rate, 200 beats/min; approximately 90% of maximum). Arterial O2 tension and saturation were maintained near resting value but CO2 tension decreased markedly with exercise, and because of increased hemoglobin concentration, arterial O2 content rose. Concomitantly, phrenic venous O2 tension, saturation and content decreased markedly (23.6 +/- 1 mm Hg, 24.5 +/- 2%, 5.2 +/- 0.3 ml/dl at 3 min of exertion) and significant fluctuations did not occur as exercise duration progressed to 30 min. Diaphragmatic arteriovenous O2 content difference and O2 extraction rose from 4 +/- 0.3 to 16 +/- 0.5 ml/dl and from 30 +/- 3 to 75 +/- 1% at 3 min of exercise, and significant deviations did not occur as exercise duration progressed. Arterial lactate and ammonia levels increased during exercise, indicating their release from working limb muscles. Phrenic-venous values of lactate and ammonia did not exceed arterial values. Ponies sweated profusely and were unable to keep up with the belt speed in the last 4 to 5 min of exercise. Constancy of phrenic arteriovenous O2 content difference in exercise indicated ability to adjust perfusion in diaphragm so as to adequately meet its O2 needs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerobiosis↗
PubMed2001

PRL receptor-mediated effects in female mouse adipocytes: PRL induces suppressors of cytokine signaling expression and suppresses insulin-induced leptin production in adipocytes in vitro.

PRL has been reported to regulate fat metabolism in several species. We recently reported PRL receptor (PRLR) expression in mouse adipocytes and increased levels of PRLR expression in the adipose tissue of lactating and PRL-transgenic mice compared with controls. These results suggest PRLR-mediated effects in adipose tissue. However, to date most studies have been performed in vivo, and it is unclear whether PRL has direct effects on adipocytes. The PRLR belongs to the cytokine receptor family, and a family of suppressors of cytokine signaling (SOCS) was recently identified. The present study was performed to investigate whether PRL has direct effects on adipocytes. The expression of cytokine-inducible SH2-domain-containing protein (CIS), SOCS-3, and SOCS-2 mRNA and protein was analyzed using ribonuclease protection assay and immunoblotting, respectively. Ovine PRL induced CIS mRNA expression and a combination of oPRL and insulin induced SOCS-3 mRNA expression in adipocytes cultured in vitro for 0-240 min, demonstrating PRLR-mediated direct effects in these cells. Furthermore, CIS, SOCS-3, and SOCS-2 mRNA and protein were all transiently expressed in adipose tissue obtained from female mice stimulated with oPRL (1 microg/g BW) for 0-24 h. In adipose tissue of female mice with endogenously high PRL levels, PRL-transgenic mice, only SOCS-2 expression was increased. The level of SOCS-2 mRNA was also increased in adipose tissue during pregnancy and lactation compared with that in wild-type virgin female mice. A possible reason for increased SOCS-2 expression after prolonged PRL exposure during lactation and in the PRL transgenes could be to restore the sensitivity of adipose tissue to PRL. In addition, the direct effect of PRL on leptin production was investigated in adipocytes cultured in vitro for 6 h. PRL inhibited insulin-induced leptin production in vitro. However, PRL had no effect on leptin production in the absence of insulin. In contrast, serum leptin concentrations were increased in PRL-transgenic females compared with control mice. In conclusion, our results demonstrate functional PRLRs in mouse adipocytes and suggest a role for CIS, SOCS-3, and SOCS-2 in regulating PRL signal transduction in adipose tissue.

Adipocytes↗
PubMed1991

Regulation of hepatic lactate balance during exercise.

The rate of exchange of lactate across the liver gives important insights into intracellular processes during muscular work. At the onset of exercise hepatic glycogenolysis increases rapidly, resulting in high rates of glycolytic flux and a transient rise in lactate output. With increasing exercise duration, gluconeogenesis is accelerated and the liver gradually shifts from a lactate-producing to a lactate-consuming state. Exercise-induced changes in hormone levels are critical in the regulation of hepatic glycogenolysis and gluconeogenesis and, therefore, net hepatic lactate balance. The fall in insulin stimulates hepatic glycogenolysis, glycolytic flux, and, as a result, hepatic lactate output. On the other hand, the stimulatory effects of glucagon on gluconeogenesis elicit an increase in hepatic lactate uptake. The rise in epinephrine may regulate gluconeogenesis during prolonged exercise by stimulating peripheral lactate mobilization, thereby providing gluconeogenic substrate to the liver. Chronic hepatic-denervation leads to an increase in gluconeogenesis and net hepatic lactate uptake at rest without altering total glucose production. However, the response to exercise is unaffected by the absence of hepatic nerves. Hence, the direction and magnitude of the hepatic lactate balance during exercise yields important information regarding flux through the gluconeogenic and glycolytic pathways, such that high rates of gluconeogenesis correspond to accelerated rates of hepatic lactate uptake and high rates of hepatic glycolytic flux lead to increased rates of hepatic lactate output.

Animals↗
PubMed1988

Gluconeogenic pathway in liver and muscle glycogen synthesis after exercise.

To determine whether prior exercise affects the pathways of liver and muscle glycogen synthesis, rested and postexercised rats fasted for 24 h were infused with glucose (200 mumol.min-1.kg-1 iv) containing [6-3H]glucose. Hyperglycemia was exaggerated in postexercised rats, but blood lactate levels were lower than in nonexercised rats. The percent of hepatic glycogen synthesized from the indirect pathway (via gluconeogenesis) did not differ between exercised (39%) and nonexercised (36%) rats. In red muscle, glycogen was synthesized entirely by the direct pathway (uptake and phosphorylation of plasma glucose) in both groups. However, only approximately 50% of glycogen was formed via the direct pathway in white muscle of exercised and nonexercised rats. Therefore prior exercise did not alter the pathways of tissue glycogen synthesis. To further study the incorporation of gluconeogenic precursors into muscle glycogen, exercised rats were infused with either saline, lactate (100 mumol.min-1.kg-1), or glucose (200 mumol.min-1.kg-1), containing [6-3H]glucose and [14C(U)]lactate. Plasma glucose was elevated one- to twofold and three- to fourfold by lactate and glucose infusion, respectively. Plasma lactate levels were elevated by about threefold during both glucose and lactate infusion. Glycogen was partially synthesized via an indirect pathway in white muscle and liver of glucose- or lactate-infused rats but not in saline-infused animals. Thus participation of an indirect pathway in white skeletal muscle glycogen synthesis required prolonged elevation of plasma lactate levels produced by nutritive support.

Animals↗
PubMed1994

Patterns of cyclic AMP binding in normal human breast.

Cyclic AMP binding proteins have been measured in normal breast tissue, in a variety of physiological conditions including resting state (69 cases), pregnancy (15 cases), lactation (4 cases), post-lactational involution (6 cases), and prolonged involution (10 cases). Levels varied greatly within the groups but median values were elevated in pregnancy, lactation, and post-lactational involution as compared with the resting and prolonged involutionary states. The proportion of different types of cyclic AMP binding proteins also differed between groups. Resting breast showed approximately equal amounts of type I and II whereas pregnant and postlactational involuting breast tissue had an increased proportion of type I binding, and the prolonged involutionary state tended to be associated with low type I. Within the subgroup of nulliparous resting breasts, the proportion of type I cyclic AMP binding protein was significantly elevated during the second half of the menstrual cycle compared with the first (p < 0.05). There were also significant positive associations between the level of epithelial proliferation and both total (p < 0.015) and type I (p < 0.002) cyclic AMP binding. This represents the strongest of association thus far reported between signalling systems and proliferation in the normal breast.

Breast↗
PubMed1984

Effects of acute hypobaric hypoxia on acid-base status of fowl blood.

Arterial blood Po/, Pco2, lactate levels and Cl- ion concentration as well as pH were measured on the time course in chickens (Gallus domesticus) as they settled in normoxic conditions and during exposure to acute hypobaric hypoxia (Pb = 450 Torr). Hypoxia provoked at first a CO2 increased output from blood and a brief stage of deep metabolic acidosis during which lactate levels suddenly increased. This acidosis was then compensated producing a return to the initial pH and a decrease in [HCO3-] + [CO3(2-)] after 60 min. Subsequently respiratory alkalosis associated with an increase in [HCO-3] + [CO3(2-)], a decrease in cl- ion concentration and a small decrease in lactate levels were observed. Prolonged exposure to hypoxia (16 h) resulted in a new return to the initial pH, a decrease in concentration of [HCO3-] + [CO3(2-)] and a high lactate level. The hematocrit value, the Hb concentration, and the plasma Na+, K+, Ca++ and Mg++ ion concentration did not change significantly.

Acid-Base Imbalance↗
PubMed1985

Role of nipple stimulation in the suppression of estrous cyclicity during extended lactation in the rat.

The role of nipple stimulation in the suppression of the estrous cycle during extended lactation was studied in rats subjected to either total, partial, or sham excision of the nipples. Each female cohabited with 4 pups, 4-14 days old, over a period of 70 days postpartum, during which vaginal smears were recorded daily. Initially, regardless of the presence of nipples, all rats exhibited a postpartum diestrus that lasted for 12-20 days. Intact females (bearing 6 pairs of nipples) continued to exhibit successive prolonged diestrous phases over 70 days of lactation. A comparable result was obtained with females bearing only the anterior pair of nipples, which, in a separate experiment, was found to be the most frequently suckled pair. However, females devoid of nipples resumed regular (4-day) estrous cycles between Days 12 and 27 postpartum, in spite of their continuous contact with pups. Thus, when lactation is prolonged beyond the normal time of weaning (Day 21 postpartum), stimulation of the nipples by sucking becomes indispensable for the continued arrest of the estrous cycle. The possible mechanisms underlying this phenomenon are discussed.

Animals↗