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PubMed1985

Studies in human lactation: zinc, copper, manganese and chromium in human milk in the first month of lactation.

Zinc, copper, manganese and chromium were measured in a total of 259 samples of human milk from 11 women from day of delivery to 31 days postpartum. Milk intakes by their fully breast-fed infants were calculated from 24-h test-weighing measurements. Zinc was analyzed by flame atomic absorption spectrophotometry, and the other elements by graphite furnace atomic absorption. Mean (+/- SD) concentrations declined from a maximum of 11.5 +/- 4.7 micrograms/ml at 2 days to 2.98 +/- 0.78 micrograms/ml at 28 +/- 3 days. Changes in the other three elements were irregular. The average copper concentration declined from 0.6 +/- 0.12 micrograms/ml on day 5 to 0.41 +/- 0.04 micrograms/ml at 28 days. Manganese levels decreased from a mean of 5.4 +/- 1.6 ng/ml on day 1 to 2.7 +/- 1.6 ng/ml on day 5; from 8 to 28 days there was little change, the overall mean being 3.7 +/- 2.2 ng/ml. The average concentration of chromium over the whole period was 0.27 +/- 0.10 ng/ml. Average daily intakes of the elements, by the infants, over the one month period were: zinc, 2.0 mg; copper, 0.25 mg; manganese, 2.0 micrograms; chromium, 150 ng.

Adult↗
PubMed1987

Studies in human lactation 3: molybdenum and nickel in human milk during the first month of lactation.

Molybdenum and nickel were measured in 62 and 46 samples, respectively, of human milk collected from 13 women between delivery and 38 d postpartum. Trace elements were analyzed by graphite-furnace atomic absorption spectrophotometry, with standard additions to whole milk without pretreatment. Molybdenum levels (mean +/- SD) fell from 15.0 +/- 6.1 ng/mL on day 1 to an apparently constant level of 1-2 ng/mL by 1 mo. Nickel concentrations did not change with time; the overall mean was 1.2 +/- 0.4 ng/mL. Intakes of the elements by infants were calculated with test-weighing data on the fully breast-fed infants of these same mothers. By 1 mo, the average daily intake of molybdenum was 1.5 micrograms; that of nickel was 0.8 microgram.

Breast Feeding↗
PubMed2002

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗
PubMed1981

Metabolism of 3H- and 14C-labelled lactate in starved rats.

1. [2-(3)H,U-(14)C]- or [3-(3)H,U-(14)C]-Lactate was administered by infusion or bolus injection to overnight-starved rats. Tracer lactate was injected or infused through indwelling cannulas into the aorta and blood was sampled from the vena cava (A-VC mode), or it was administered into the vena cava and sampled from the aorta (V-A mode). Sampling was continued after infusion was terminated to obtain the wash-out curves for the tracer. The activities of lactate, glucose, amino acids and water were followed. 2. The kinetics of labelled lactate in the two modes differed markedly, but the kinetics of labelled glucose were much the same irrespective of mode. 3. The kinetics of (3)H-labelled lactate differed markedly from those for [U-(14)C]lactate. Isotopic steady state was attained in less than 1h of infusion of [(3)H]lactate but required over 6h for [U-(14)C]lactate. 4. (3)H from [2-(3)H]lactate labels glucose more extensive than does that from [3-(3)H]lactate. [3-(3)H]Lactate also labels plasma amino acids. The distribution of (3)H in glucose was determined. 5. Maximal radioactivity in (3)HOH in plasma is attained in less than 1min after injection. Near-maximal radioactivity in [(14)C]glucose and [(3)H]glucose is attained within 2-3min after injection. 6. The apparent replacement rates for lactate were calculated from the areas under the specific-radioactivity curves or plateau specific radioactivities after primed infusion. Results calculated from bolus injection and infusion agreed closely. The apparent replacement rate for [(3)H]lactate from the A-VC mode averaged about 16mg/min per kg body wt. and that in the V-A mode about 8.5mg/min per kg body wt. The apparent rates for [(14)C]lactate (;rate of irreversible disposal') were 8mg/min per kg body wt. for the A-VC mode and 5.5mg/min per kg body wt. for the V-A mode. Apparent recycling of lactate carbon was 55-60% according to the A-VC mode and 35% according to the V-A mode. 7. The specific radioactivities of [U-(14)C]glucose at isotopic steady state were 55% and 45% that of [U-(14)C]lactate in the A-VC and V-A modes respectively. We calculated, correcting for the dilution of (14)C in gluconeogenesis via oxaloacetate, that over 70% of newly synthesized glucose was derived from circulating lactate. 8. Recycling of (3)H between lactate and glucose was evaluated. It has no significant effect on the calculation of the replacement rate, but affects considerably the areas under the wash-out curves for both [2-(3)H]- and [3-(3)H]-lactate, and calculation of mean transit time and total lactate mass in the body. Corrected for recycling, in the A-VC mode the mean transit time is about 3min, the lactate mass about 50mg/kg body wt. and the lactate space about 65% of body space. The V-A mode yields a mass and lactate space about half those with the A-VC mode. 9. The area under the wash-out curve for [(14)C]lactate is some 20-30 times that for [(3)H]lactate, and apparent carbon mass is 400-500mg/kg body wt. and presumably includes the carbon of glucose, pyruvate and amino acids, which are exchanging rapidly with that of lactate.

Animals↗
PubMed1985

Genetic and phenotypic relationships between lactation cell counts and milk yield and composition of Holstein cows.

Monthly somatic cell count data were collected between February 1977 and February 1982 for Holstein cows in 928 herds enrolled on the Quebec Dairy Herd Analysis Service. The geometric mean of the log monthly cell counts was calculated for each lactation. Official lactation records for 305-day milk, fat, and protein yields, and fat and protein percents were obtained for same cows. There were 18,189 cows in first lactation representing 257 sires, 13,225 in second lactation representing 206 sires, and 8,683 in third lactation representing 151 sires. Heritabilities of yield traits and protein percent increased across three lactations. Heritability of fat percent was similar in first and third lactations but decreased slightly in second lactations. Heritability of lactation cell count was small, being least in second lactations. Genetic correlations between lactation cell count and yield traits were positive in first lactations, small and negative in second lactations, and small and positive in third lactations. Genetic correlations between lactation cell count and fat and protein contents were small in the three lactations. Phenotypic correlations between lactation cell count and production traits were small in each of the three lactations. Genetic correlations between yield traits in early lactation and lactation cell count in a subsequent lactation were positive. The genetic correlation between protein percent in an early lactation and cell count in a later lactation was large between first and second lactations, decreased between second and third lactation, and small between first and third lactations. Genetic correlations were small and negative for fat percent.

Animals↗
PubMed1985

Energy recycling by lactate efflux in growing and nongrowing cells of Streptococcus cremoris.

Streptococcus cremoris was grown in pH-regulated batch and continuous cultures with lactose as the energy source. During growth the magnitude and composition of the electrochemical proton gradient and the lactate concentration gradient were determined. The upper limit of the number of protons translocated with a lactate molecule during lactate excretion (the proton-lactate stoichiometry) was calculated from the magnitudes of the membrane potential, the transmembrane pH difference, and the lactate concentration gradient. In cells growing in continuous culture, a low lactate concentration gradient (an internal lactate concentration of 35 to 45 mM at an external lactate concentration of 25 mM) existed. The cell yield (Ymax lactose) increased with increasing growth pH. In batch culture at pH 6.34, a considerable lactate gradient (more than 60 mV) was present during the early stages of growth. As growth continued, the electrochemical proton gradient did not change significantly (from -100 to -110 mV), but the lactate gradient decreased gradually. The H+-lactate stoichiometry of the excretion process decreased from 1.5 to about 0.9. In nongrowing cells, the magnitude and composition of the electrochemical proton gradient was dependent on the external pH but not on the external lactate concentration (up to 50 mM). The magnitude of the lactate gradient was independent of the external pH but decreased greatly with increasing external lactate concentrations. At very low lactate concentrations, a lactate gradient of 100 mV existed, which decreased to about 40 mV at 50 mM external lactate. As a consequence, the proton-lactate stoichiometry decreased with increasing external concentrations of protons and lactate at pH 7.0 from 1 mM lactate to 1.1 at 50 mM lactate and at pH 5.5 from 1.4 at l mM lactate to 0.7 at 50 mM lactate. The data presented in this paper suggest that a decrease in external pH and an increase in external lactate concentration both result in lower proton-lactate stoichiometry values and therefore in a decrease of the generation of metabolic energy by the end product efflux process.

Energy Metabolism↗
PubMed1999

Continuous veno-venous haemodialysis with a novel bicarbonate dialysis solution: prospective cross-over comparison with a lactate buffered solution.

OBJECTIVE: To compare acid-base balance, lactate concentration and haemodynamic parameters during continuous veno-venous haemodialysis (CVVHD) using bicarbonate or a lactate buffered dialysate. METHODS DESIGN: prospective randomized cross-over design; SETTING: Multicentre combined adult surgical and medical intensive care units. Patients; 26 critically ill patients starting CVVHD for acute renal failure. INTERVENTIONS: Each patient to receive 48 h of bicarbonate dialysate and 48 h of lactate dialysate with the order of the 48 h block randomized at trial entry. RESULTS: The serum bicarbonate increased from baseline in both the lactate and bicarbonate groups over the first 48 h of treatment (16.3+/-1.53 to 22.2+/-1.41 mmol/l and 18.9+/-2.02 to 22.2+/-1.18 mmol/l, respectively) and continued to rise towards normal over the next 48 h after cross-over to the other dialysate. The H+ and pCO2 only trended higher in the lactate group. Unlike the acid base parameters, serum lactate levels varied depending on the dialysate composition. The patients initially randomized to the lactate dialysate had higher serum lactate levels and these tended to increase further after 48 h of dialysis from 2.4+/-0.8 to 2.6+/-0.4 mmol/l. However, in the following 48 h the lactate levels fell to 1.8+/-0.6 (P = 0.039) while patients were being treated with the bicarbonate dialysate. Similar results were seen in the patients initially randomized to the bicarbonate dialysate. Serum lactate remained stable over the first 48h (1.4+/-0.2 to 1.5+/-0.1 mmol/l) but after cross-over to the lactate dialysate increased to 3.1+/-0.7 mmol/l (P = 0.051). Overall, lactate levels were significantly higher during dialysis with lactate buffered solution than bicarbonate buffered solution (2.92+/-0.45 vs. 1.61+/-0.25 mmol/l P = 0.01). Mean arterial pressure trended higher during bicarbonate dialysis but did not reach statistical significance (lactate vs. bicarbonate; 71.1+/-3.1 vs. 81.3+/-5.8 mm Hg). Subgroup analysis of the patients with abnormal liver indices or increased lactate levels at initiation of dialysis (n = 15) revealed only a trend toward better bicarbonate control (lactate vs. bicarbonate; 22.00+/-1.73 vs. 22.86+/-1.09, P = 0.2). However, in this group with hepatic insufficiency elevations in serum lactate were even greater during lactate compared to the bicarbonate dialysis (3.39+/-0.68 vs. 1.78+/-0.42 P = 0.036). Patients who had elevations of lactate during lactate dialysis had a high mortality (6 of 7). These patients had an even greater disparity in lactate levels (4.3+/-1.4 vs. 1.3 +/-0.3) and blood pressure (68.0+/- 7.7 vs. 87.2+/-17.1) between lactate and bicarbonate dialysis. Due to small patient numbers these comparisons did not achieve statistical significance. CONCLUSION: During continuous veno venous haemodialysis a bicarbonate buffered dialysis solution provided equal acid-base control but maintained more normal lactate levels than a lactate buffered dialysis solution.

Acid-Base Equilibrium↗
PubMed1984

Lactate metabolism in the perfused rat hindlimb.

A preparation of isolated rat hindleg was perfused with a medium consisting of bicarbonate buffer containing Ficoll and fluorocarbon, containing glucose and/or lactate. The leg was electrically prestimulated to deplete partially muscle glycogen. The glucose was labelled uniformly with 14C and with 3H in positions 2, 5 or 6, and lactate uniformly with 14C and with 3H in positions 2 or 3. Glucose carbon was predominantly recovered in glycogen, and to a lesser extent in lactate. The 3H/14C ration in glycogen from [5-3H,U-14C]- and [6-3H,U-14C]-glucose was the same as in glucose. Nearly all the utilized 3H from [2-3H]glucose was recovered as water. Insulin increased glucose uptake and glycogen synthesis 3-fold. When the muscle was perfused with a medium containing 10 mM-glucose and 2 mM-lactate, there was little change in lactate concentration. 14C from lactate was incorporated into glycogen. There was a marked exponential decrease in lactate specific radioactivity, much greater with [3H]- than with [14C]-lactate. The 'apparent turnover' of [U-14C]lactate was 0.28 mumol/min per g of muscle, and those of [2-3H]- and [3-3H]-lactate were both about 0.7 mumol/min per g. With 10 mM-lactate as sole substrate, there was a net uptake of lactate, at a rate of about 0.15 mumol/min per g, and the apparent turnover of [U-14C]lactate was 0.3 mumol/min per g. The apparent turnover of [3H]lactate was 3-5 times greater. When glycogen synthesis was low (no prestimulation, no insulin), the incorporation of lactate carbon into glycogen exceeded that from glucose, but at high rates of glycogen deposition the incorporation of lactate carbon was much less than that of glucose. Lactate incorporation into glycogen was similar in fast-twitch white and fast-twitch red muscle, but was very low in slow-twitch red fibres. We find that (a) pyruvate in muscle is incorporated into glycogen without randomization of carbon, and synthesis is not inhibited by mercaptopicolinate or cycloserine; (b) there is extensive lactate turnover in the absence of net lactate uptake, and there is a large dilution of 14C-labelled lactate from endogenous supply; (c) there is extensive detritiation of [2-3H]- and [3-3H]-lactate in excess of 14C utilization.

Animals↗
PubMed1993

Lactate and H+ effluxes from human skeletal muscles during intense, dynamic exercise.

1. Lactate and H+ efflux from skeletal muscles were studied with the one-legged knee extension model under conditions in which blood flow, arterial lactate and the muscle-blood lactate concentration gradient were altered. Subjects exercised one leg twice to exhaustion (EX1, EX2), separated by a 10 min recovery and a period of intense intermittent exercise. After 1 h of recovery the exercise protocol was repeated with the other leg. Low-intensity exercise was performed with one leg during the recovery periods, while the other leg was passive during its recovery periods. 2. Prior to, and immediately after, EX1 and EX2 and then 3 and 10 min after EX1, a biopsy was taken from the vastus lateralis of the exercised leg for lactate, pH, muscle water and fibre-type determinations. Measurements of leg blood flow and venous-arterial differences for lactate (whole blood and plasma), pH, partial pressure of CO2 (PCO2), haemoglobin, saturation and base excess (BE) were performed at the end of exercise and regularly during the recovery period after EX1. 3. The lactate release was linearly related (r = 0.96; P < 0.05) to the muscle lactate gradient over a range of muscle lactate from 0 to 45 mmol (kg wet wt)-1. The muscle lactate transport was evaluated from the net femoral venous-arterial differences (V-Adiff) for lactate. This rose with increases in the muscle lactate gradients, but as the gradient reached higher levels the V-Adiff lactate responded less than at smaller gradients. Thus, the lactate transport over the muscle membrane appears to be partly saturated at high muscle lactate concentrations. 4. The percentage of slow twitch (%ST) fibres was inversely related to the muscle lactate gradient, but it was not correlated to the lactate release at the end of the exercises. In spite of a significantly higher blood flow during active recovery, the lactate release was the same whether the leg was resting or performed low-intensity exercise in the recovery periods. In several other conditions the muscle lactate and H+ gradients would have predicted that the V-Adiff lactate would have been greater than it actually was. Thus, a variety of factors affect muscle lactate transport, including arterial lactate concentration, muscle perfusion, muscle contraction pattern and muscle morphology. 5. The muscle and femoral venous pH declined during EX1 to 6.73 and 7.14-7.15, respectively, and they increased to resting levels during 10 min of either passive or active recovery.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗