Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LACTATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMed1996

Serum lactate is not predicted by anion gap or base excess after trauma resuscitation.

OBJECTIVE: The inability to normalize lactate predicts death after trauma, but lactate may not be immediately available in every center. We postulated that, in a normal acid-base environment, lactate would correlate with the anion gap and the base excess of an arterial blood gas. METHODS: We studied 52 consecutive, invasively monitored patients with trauma admitted directly to the intensive care unit (ICU) from the emergency department or operating room in our level I center to determine whether base excess and anion gap could predict lactate. Lactate, base excess, and anion gap were recorded upon admission to the ICU and 8, 16, 24, 36, and 48 hours after admission. Correlation coefficients (r2) were calculated for the total patients, the 43 survivors, and the nine non-survivors. RESULTS: Serum lactate was significantly higher in nonsurvivors at 16 hours after post ICU admission (4.0 +/- 1.69 vs. 2.84 +/- 1.49, p < 0.05), and this trend persisted; the greatest difference was seen at 48 hours after admission (2.92 +/- 1.47 vs. 1.76 +/- 0.57, p < 0.001). There were no differences in base excess or anion gap between survivors and nonsurvivors. We found no consistent correlation between lactate versus anion gap, lactate versus base excess, or anion gap versus base excess. CONCLUSIONS: There is no correlation between lactate, base excess, and anion gap after initial resuscitation. Neither anion gap nor base excess was capable of predicting lactate; therefore, lactate must be directly measured. The lack of correlation of anion gap with base excess or lactate suggests the presence of unmeasured anions, an impairment in acid-base regulation after injury and resuscitation, or both.

Acid-Base Equilibrium↗
PubMed1995

Dissociation between behavioral and hormonal responses to the forced swim stress in lactating rats.

Retention of immobility in the Porsolt forced swim test is believed to be dependent upon glucocorticoid secretion in male rats. Because lactating females exhibit increased basal glucocorticoid secretion and blunted stress responses, we tested the hypothesis that lactation-induced changes in adrenal glucocorticoid and in circulating estrogen and progesterone levels would improve retention and/or acquisition of immobility. Immobility was recorded during 3 intervals of 5 min on day 1 (acquisition) and one 5 min interval 24 h later (retention). Blood samples were collected before the swim test and at various times after the onset of stress for plasma ACTH and corticosterone (B) determinations. Male rats (young=200 g, old=325 g) were compared to virgin females (V) and to lactating females in early (day 8-10, EL) and late (day 17-19, LL) lactation. Adrenalectomy (ADX) and ovariectomy (OVX) were performed 5 and 10 days prior to testing, respectively. All animals acquired immobility at the end of the 15 min swim on day 1, but only the young male group exhibited a significant retention of immobility on day 2. Total immobility was higher in males than females (V) although basal and stress-induced ACTH and B secretion were comparable on both testing days. Lactational status did not affect immobility in either the acquisition or retention phases. However, stress-induced ACTH secretion was greatly diminished in intact and ADX lactating females (EL and LL) compared to virgins (LL < EL < virgin), demonstrating a clear dissociation between behavioral and neuroendocrine responses. Following ADX, immobility in the retention phase was either decreased in males or increased in lactating females. Finally, OVX decreased immobility in both lactating (EL) and virgin females without significantly altering the magnitude of the ACTH and B responses to stress. In summary, our results demonstrated both sex-related and lactation-related differences in the behavioral and endocrine responses to he forced swim test of Porsolt. Although retention of the immobile response is thought to involve glucocorticoids and/or opioids secreted during the first testing session, we did not find evidence for a direct relationship between basal or stress-induced total corticosterone secretion, the magnitude of ACTH response to stress and behavioral scores in the retention period. However, experimental variables such as body weight, sex and water depth could significantly modify the outcome of behavioral testing and question the validity of glucocorticoid-mediated retention processes. Since the effect of ADX was reversed in lactating females compared to male rats, we hypothesize that glucocorticoid sensitivity of cognitive processes controlling behavioral reactivity is different from that controlling hypothalamic-adrenocortical function. Our results also demonstrated a clear dissociation between behavioral and neuroendocrine responses to the swim test, in particular during lactation. In early and late lactation, blunted responsiveness to stress was not caused by enhanced glucocorticoid feedback but might result from modifications in the inhibitory and/or stimulatory inputs to hypothalamic neurons controlling adrenocortical activity.

Adrenalectomy↗
PubMed2004

Role of leptin in orexigenic neuropeptide expression during lactation in rats.

The expression of neuropeptide Y (NPY) and agouti-related peptide (AgRP), both of which are important neuropeptides involved in regulation of energy balance and hormone secretion, is up-regulated in the arcuate nucleus during lactation in rodents. The present study tested whether reductions in circulating insulin and/or leptin that occur in lactation provide the critical signals to these systems. Lactating female rats received 3-day infusions of either bovine insulin or recombinant rat leptin via Alzet Osmotic minipumps implanted subcutaneously in regimens designed to restore serum concentrations of these hormones to the higher non-lactating level. Compared to non-lactating rats in diestrus, lactating rats displayed significantly lower serum concentrations of insulin and leptin, and significantly increased NPY peptide concentrations in the paraventricular nucleus (PVN) and median eminence, and AgRP mRNA in the arcuate nucleus. Infusion of leptin in lactating females significantly increased serum concentrations of leptin and significantly reduced NPY concentrations in the PVN and median eminence, and decreased NPY and AgRP mRNAs in the arcuate nucleus. The same effects were produced by infusion of insulin in lactating rats, which restored both insulin and leptin concentrations in serum. The levels of pro-opiomelanocortin mRNA in the arcuate nucleus were not different in non-lactating and lactating females, and were not altered by leptin or insulin treatment. These findings support the hypothesis that the reduction in circulating leptin during lactation contributes to increased expression of NPY and AgRP in hypothalamic systems involved in the behavioural and neuroendocrine adaptations to lactation.

Agouti-Related Protein↗
PubMed1995

The contribution of glucose cycling to the maintenance of steady-state levels of lactate by hepatocytes during glycolysis and gluconeogenesis.

When hepatocytes from fasted rats were incubated with 10 mM glucose, there was a linear accumulation of lactate and pyruvate for about 80 min after which steady-state concentrations of these metabolites became established. The rate of glycolysis, determined with [6-3H]glucose, was constant over the entire incubation period and was 50% greater than that calculated from carbon balance studies. This suggests that one-third of the glycolytic products formed were recycled to glucose. To enable study of the factors associated with the generation and maintenance of the lactate steady state and to measure accurately the carbon balance, incubations were performed using supraphysiological concentrations of glucose (20-80 mM). Under these conditions the initial rate of lactate accumulation and its concentration at steady state were shown to be dependent on the concentration of extracellular glucose. Rates of glycolysis were also measured using 40 mM [6-3H]glucose and [U-14C]glucose added alone, or in combination with a steady-state lactate concentration (3 mM). There was no effect on the rate of glycolysis determine with [6-3H]glucose, even when lactate was present in the medium. The difference in rates between measurements with the two isotopes reflect the apparent degree of glucose recycling which in the absence and presence of added lactate increased from 0.26 to 0.54 mumol C3 equivalents min-1.g-1 respectively. Identical studies employing [U-14C]lactate showed that glucose and CO2 were the major products of lactate metabolism under steady-state conditions and that the formation of lactate from [U-14C]glucose exactly balanced the rate of lactate removal as a result of oxidation and gluconeogenesis. These studies provide evidence for the concomitant operation of glycolysis and gluconeogenesis, even in the presence of high glucose concentrations. They also demonstrate that lactate steady states are achieved not by the cessation of glycolysis but rather by the removal of lactate and pyruvate at a rate equal to that of their production.

Animals↗
PubMed1993

Na+/H+ exchange inhibitors reverse lactate-induced depression in postischaemic ventricular recovery.

1. By use of pharmacological approaches, the present study examined the hypothesis that the deleterious effect of lactate on postischaemic ventricular recovery may be mediated, at least in part, by enhanced activation of the Na+/H+ exchanger at the time of reperfusion. 2. Spontaneously beating isolated hearts of the rat were subjected to 15 min zero-flow global ischaemia followed by 30 min reperfusion. The effects of lactate (10, 20 or 40 mM) were studied by adding it 20 min before ischaemia whereas reperfusion was carried out with lactate-free buffer. 3. Pretreatment with 20 or 40 mM lactate significantly reduced postischaemic recovery of developed force to 17 +/- 3% and 16 +/- 4% of preischaemic values (P < 0.05) compared to a 78 +/- 4% recovery in control hearts. Similarly, recovery in ventricular rate was significantly reduced to 34 +/- 7.6% and 38 +/- 12% with 20 and 40 mM lactate, respectively compared to 97.5 +/- 6.4% recovery in control hearts. At a concentration of 10 mM, lactate was without effect on either force or ventricular rate recovery. 4. Coadministration of either of two Na+/H+ exchange inhibitors, amiloride (174 microM) or 5-N,N-hexamethylene amiloride (HMA, 1 microM) with lactate and inclusion of the two drugs during the first 5 min of reperfusion resulted in reversal of lactate-induced inhibition of force recovery with observed recoveries of 69 +/- 6.7% and 64 +/- 5% with amiloride and HMA, respectively. Similarly, recovery in ventricular rate was significantly enhanced to 92 +/- 10% and 89 +/- 6% with amiloride and HMA, respectively compared to 38 +/- 12% recovery in control hearts. In the presence of amiloride or HMA, force recovery in lactate-treated hearts was significantly increased to 68 +/- 16% and 72 +/- 4.7% of preischaemic values, respectively.6. In spontaneously beating hearts, resting tension changes during both ischaemia and reperfusion were not statistically different between treatment groups. However, in paced hearts pretreated with 40 mM lactate the elevation in resting tension during the first 5 min of reperfusion, was significantly reduced by both amiloride and HMA.7. Changes in functional recoveries produced by either lactate or Na+/H+ exchange inhibitors were unrelated to alterations in high energy phosphate depletion during ischaemia or to repletion of these compounds after 30 min reperfusion either in spontaneously beating or electrically paced hearts.8. The results suggest that stimulated Na'/H+ exchange activation at reflow contributes, at leastpartially, to lactate-induced depression of postischaemic recovery.

Amiloride↗
PubMed1999

Dietary supplements for the lactating mother: influence on the trace element content of milk.

Milk production is a complex process where nutritional factors interact with structural hormonal and behavioural influences. In recent years important advances have been made in understanding the role of the nutritional status of lactating women on the outcome of breastfeeding. Many questions remain unanswered about the exact requirement of trace elements for lactating mothers. The effect of dietary zinc, copper and iodine supplements on the milk concentration of these micronutrients was studied. The supplementation trial employed a specific balanced nutritional supplement prepared for the nursing mothers. The study was carried out on women living in Ferrara and its surrounding area. The population under study was healthy Italian mothers, of good socioeconomic status, and their normal infants. In total, 32 women were enrolled in the study and 22 completed it. The infants (9F, 13M) were full-term, healthy singletons and were put to breast within 12 h of birth. All women who finished the study completed a 3 d dietary record. Nutrient analysis revealed the following mean daily dietary trace element intake in the lactating mothers: zinc = 12 mg, copper = 1.4 mg and iodine = 145 microg. The zinc and copper dietary intake was in agreement with the daily intake proposed for nursing Italian mothers, while the daily intake of iodine was below the recommended intake of 200 microg. The breastfeeding mothers were placed in 2 groups, with 7 primiparas and 4 multiparas per group: lactating women eating a traditional Italian diet without vitamin and mineral supplements, and lactating women enrolled in the nutrification programme and given a nutritional supplement to their traditional diet. The supplement (PerMamma Abbott) provided 20mg zinc sulfate, 2mg copper sulfate and 116 microg potassium iodide. These quantities cover about 60-90% of the recommended intake for nursing Italian mothers. Samples of 10 ml of milk were collected at 3, 30, 90d postpartum. Zinc milk concentrations declined significantly over the study period for all lactating subjects, without differences in the rate of decline between the women who started supplementation during lactation and those who did not. Copper did not change during the first month of lactation, then declined at day 90 in supplemented and unsupplemented women, without significant differences between the two groups. An early sharp decline in milk iodine occurred in all lactating subjects, independently of iodine supplementation. After the first month of lactation breast milk iodide levels remained stable in all subjects under study. No significant differences between the two study groups were observed. The lack of correlation between the iodide level in breast milk and maternal dietary intake of iodine is not in agreement with previously published reports. The present results indicate that in healthy, well-nourished lactating Italian women, whose diet is adequate, the levels of zinc, copper and iodine in milk are not influenced by short-term supplementary intakes and that the milk levels of the trace elements studied are maintained over different levels of intake. Further research and examination by longitudinal studies are needed to establish the exact relationship between the amount of iodine furnished to the nursing mother and the iodine content of human milk. The role of compensatory homeostatic mechanisms which act during lactation needs further consideration and closer scrutiny.

Analysis of Variance↗
PubMed1991

Lactate transport in skeletal muscle cells: uptake in L6 myoblasts.

During exercise, lactate is produced by degradation of glucose-6-phosphate during glycolysis in the contracting muscles. This lactate is metabolized during and after exercise in the muscle itself and also in the liver and other muscles, which can use it as an energy metabolite or can resynthetize glycogen. Lactate is transported in the blood, and the rate of muscular utilization may be limited by two factors: the rate of metabolic utilization by the muscle cell; and the rate of transport across the membrane regulating lactate transfer from the blood to the cell. We have studied lactate uptake in L6 muscle cells by incorporation of 14C-lactate. The uptake rates were linear for 20 seconds with 5 mM lactate and 10 seconds with 20 mM. The uptake during 10 seconds for physiological lactate concentrations (1-20 mM) gave a straight line passing through the origin. Lactate uptake was not altered by specific inhibitors of lactate transport (2.5 mM alpha cyano-4-hydroxycinnamic acid. 5 microM 4,4'-diisothiocyanostilbene-2,2'disulphonic acid) or by the stereospecific D-lactate inhibitor. The results suggest that L-lactate uptake in L6 cells occurs by passive diffusion.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

Lactate transport in rat sarcolemmal vesicles and intact skeletal muscle, and after muscle contraction.

To determine whether it was possible to measure lactate transport rates into intact skeletal muscles, the transport of lactate (zero-trans) was determined in soleus muscle strips incubated in vitro and compared with lactate transport in sarcolemmal vesicles. In addition, the effects of muscle contractility on lactate transport were investigated in electrically-stimulated soleus muscle strips. In both the intact muscle and the sarcolemmal preparations the rates of transport were saturable, stereospecific, and inhibitable by monocarboxylates (pyruvate, alpha-cyano-4-hydroxycinnamate) and a protein modifier (N-ethylmaleimide; P < 0.05). The anion exchange inhibitor SITS had no effect on lactate uptake (P > 0.05). In both preparations lactate transport followed an inwardly directed proton gradient. Relative comparisons (%) between the preparations indicated a similar slope of increasing transport rates with increasing lactate concentrations and similar responses to a changing pH environment. These characterizations of L-lactate transport into isolated sarcolemmal vesicles and muscle strips revealed that both preparations yielded similar conclusions regarding the transmembrane movement of L-lactate. By using this more physiological muscle preparation, contractile activity, induced by electrical stimulation, did not increase lactate uptake in skeletal muscle in the post-exercise period whereas under similar conditions a marked increase in 2-deoxy-D-glucose uptake occurred (+ 47%; P < 0.05). These data suggest that the transport of glucose and lactate in contracting muscle is regulated differently. These studies also show that the incubated muscle strip preparation may be useful for studying lactate transport in an intact cell system during physiological experiments.

Animals↗
PubMed1973

The effect of exercise on lactate metabolism.

1. An I.V. injection of 5 muc [U-(14)C]sodium L(+)-lactate was given to four subjects at rest and again 10 min after beginning a 40-50 min period of heavy exercise at an estimated 62-72% of their maximum aerobic power (V(O) (2) max.). Both blood lactate concentration and V(O) (2) remained relatively constant after the first few minutes of exercise.2. In all subjects both at rest and during exercise blood lactate and total radioactivity were measured at frequent intervals after injection of [(14)C]lactate. Timed expired gas collections were made and the quantity of (14)CO(2) present in each collection measured. In two subjects the specific activity of lactate and of glucose isolated from blood was also measured.3. It was found that during 30 min of exercise 35-68% of the administered [(14)C]lactate was recovered as (14)CO(2) in the expired gas, whereas at rest only 3-7% was recovered in the same period.4. After injection of [(14)C]lactate the blood (14)C concentration and the specific activity of the blood lactate declined very rapidly. This decline was more rapid during exercise than at rest.5. In the two subjects in whom it was measured the specific activity of blood glucose was lower during exercise than at rest.6. These results show that both at rest and during heavy exercise, lactate is removed from the blood and metabolized, and that during exercise this metabolism is much more rapid.7. In the light of these findings the sustained blood lactate concentration observed in these experiments is regarded as representing a dynamic equilibrium between the production and metabolism of lactate during exercise. The results give no support to the hypothesis that lactate is produced only during the first few minutes of submaximal work.

Blood Glucose↗
PubMed1981

Control of fluid intake in pregnant and lactating rats.

1. During 24 hr water deprivation, the pregnant and lactating rats lost more weight than the non-mated animals. The increase in haematocrit was considerably greater in the lactating animals although plasma osmolality increased to the same extent in both lactating and non-mated animals. 2. Following water deprivation, the water intake of the lactating rats was significantly less than that of the pregnant, post-lactating or non-mated animals when expressed as a percentage of the weight loss during dehydration. While the non-mated rats restored their plasma osmolality to the pre-deprivation value upon drinking, the lactating rats sustained a new decrease in osmolality despite the fact that their mean haematocrit was still elevated. 3. When the dehydrated animals were given isotonic saline to drink instead of water, both lactating and non-mated animals restored their body weight and haematocrit to pre-deprivation levels. 4. Lactating rats showed a reduced absolute and net fluid intake in response to I.V. hypertonic saline which could not be explained by more rapid renal clearance of the solute. 5. The pregnant and lactating rats drank less in response to s.c. isoprenaline than did the post-lactating and non-mated animals. 6. The spontaneous 3 hr fluid intake was significantly less during lactation. 7. It is suggested that during the hours of daylight, lactating rats are less responsive to dipsogenic stimuli arising from deficits in both their intracellular and extracellular fluid spaces.

Animals↗
PubMed1994

Lactate efflux from fatigued fast-twitch muscle fibres of Xenopus laevis under various extracellular conditions.

1. Isolated, fast-twitch, low-oxidative muscle fibres from the iliofibularis muscle of Xenopus laevis were fatigued by intermittent tetanic stimulation at 20 degrees C in different Ringer solutions and the amount of lactate released was determined. 2. The rate of lactate efflux was constant during 10 min of intermittent stimulation while lactate in the fibres accumulated, and lactate efflux was not hampered by an unstirred layer surrounding the isolated muscle fibre. 3. The rate of lactate efflux at extracellular pH 7.2 was the same as that at pH 7.8, but depended on the type of buffer used; the highest efflux rate (mean +/- S.E.M., 7.4 +/- 2.2 mumol min-1 (g dry weight)-1, n = 8) was observed in bicarbonate-buffered Ringer solution. This rate was about 2.5 times higher than the rate in phosphate-buffered Ringer solution (2.9 +/- 1.3 mumol min-1 (g dry weight)-1, n = 8), indicating that lactate-bicarbonate exchange is the most important route for lactate extrusion in vivo. 4. The highest rate of lactate efflux corresponds to a rate of glycolytic ATP production which is only about 30% of the oxidative rate of ATP production (calculated from the maximum rate of oxygen consumption determined previously). 5. In the presence of 5 mM alpha-cyano-4-hydroxycinnamate (CHC) the lowest lactate efflux rate (1.5 +/- 0.6 mumol min-1 (g dry weight)-1, n = 16) was found. This rate was independent of the composition of the Ringer solution. Assuming that 5 mM CHC completely inhibits lactate transporters in the sarcolemma, the rate of lactate efflux in the presence of 5 mM CHC can be explained by passive diffusion, but only if most lactate is extruded via the T-tubules.

Animals↗
PubMed1999

Homofermentative production of D- or L-lactate in metabolically engineered Escherichia coli RR1.

We investigated metabolic engineering of fermentation pathways in Escherichia coli for production of optically pure D- or L-lactate. Several pta mutant strains were examined, and a pta mutant of E. coli RR1 which was deficient in the phosphotransacetylase of the Pta-AckA pathway was found to metabolize glucose to D-lactate and to produce a small amount of succinate by-product under anaerobic conditions. An additional mutation in ppc made the mutant produce D-lactate like a homofermentative lactic acid bacterium. When the pta ppc double mutant was grown to higher biomass concentrations under aerobic conditions before it shifted to the anaerobic phase of D-lactate production, more than 62.2 g of D-lactate per liter was produced in 60 h, and the volumetric productivity was 1.04 g/liter/h. To examine whether the blocked acetate flux could be reoriented to a nonindigenous L-lactate pathway, an L-lactate dehydrogenase gene from Lactobacillus casei was introduced into a pta ldhA strain which lacked phosphotransacetylase and D-lactate dehydrogenase. This recombinant strain was able to metabolize glucose to L-lactate as the major fermentation product, and up to 45 g of L-lactate per liter was produced in 67 h. These results demonstrate that the central fermentation metabolism of E. coli can be reoriented to the production of D-lactate, an indigenous fermentation product, or to the production of L-lactate, a nonindigenous fermentation product.

Acetate Kinase↗
PubMed1992

Glyconeogenic and oxidative lactate utilization in skeletal muscle.

In this article we present a synthesis of recent information concerning the fate of lactate in skeletal muscle. This is important since lactate is continuously produced by skeletal muscle at rest and at all levels of exercise. Therefore, the disposal of lactate as an 'intermediary' metabolite is discussed. The two primary fates of lactate in skeletal muscle are (1) oxidation and (2) glycogen synthesis (glyconeogenesis). From recent evidence it seems relatively clear that glycogen formation in muscle is primarily dependent on glucose, although in fast twitch muscles a considerable proportion of lactate can account for muscle glycogen formation, especially immediately after exercise when circulating lactate levels are elevated. Exactly how lactate is converted to glycogen is not known yet, but an extramitochondrial pathway that is divergent from the hepatic gluconeogenic pathway seems likely. Oxidation of lactate is quantitatively the most important means of disposing of lactate, whether in exercising or nonexercising muscle. The lactate gradient between muscle and blood may be an important factor dictating whether lactate is taken up or released by muscle, independent of whether the muscle is active or not. Finally a novel role for epinephrine is considered that may be important for the mitochondrial oxidation of lactate.

Animals↗
PubMed1978

Glucose lactate interrelations in sheep.

The constant-infusion, isotope-dilution method was used to investigate the interrelationships between the glucose and lactate pools of six trained sheep deprived of food overnight. Arterial plasma lactate concentration was a linear function of the net lactate entry rate as was the net production of glucose from lactate, which suggests that the net rate of formation of glucose from lactate is dependent on the availability of lactate. Similarly the arterial plasma glucose concentration was correlated with the net entry rate of glucose as was the net production rate of lactate from glucose, suggesting that the net rate of lactate production from glucose is a function of arterial plasma glucose concentration. The demonstration of these two interrelations between glucose and lactate in normal sheep suggests that, in the absence of external factors producing hormonal or other changes that could cause perturbations of carbohydrate homeostasis, the net rates of conversion of glucose to lactate and of lactate to glucose may be largely determined by the arterial concentrations of glucose and lactate, respectively.

Animals↗
PubMed1989

Insulin inhibition of overnight glucose production and gluconeogenesis from lactate in NIDDM.

Increased gluconeogenesis contributes to fasting hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM). We examined whether insulin inhibits gluconeogenesis from lactate by altering the fate of lactate and/or by reducing lactate flux. Seven patients with NIDDM (age 51 +/- 4 yr, body mass index 28 +/- 2 kg/m2) were studied before and 3 wk after achieving normoglycemia with evening insulin therapy. Basal glucose production (Ra) and utilization were measured overnight [( 3-3H]glucose infusion from 9 P.M. to 8 A.M.) and lactate turnover and conversion to glucose between 4 and 8 A.M. [( U-14C]lactate infusion) before and after insulin therapy. During insulin therapy, fasting plasma glucose decreased from 188 +/- 13 to 99 +/- 7 mg/dl (P less than 0.001) due to inhibition of glucose Ra from 3.0 +/- 0.1 to 2.2 +/- 0.1 mumol.kg-1.min-1 (P less than 0.005). Plasma free insulin increased from 6 +/- 1 to 11 +/- 1 microU/ml (P less than 0.005). Plasma lactate concentrations (1.1 +/- 0.2 vs. 1.0 +/- 0.1 mmol/l before vs. after insulin therapy) and the lactate turnover rate (15.6 +/- 0.9 vs. 14.2 +/- 0.8 mumol.kg.min) remained unchanged, whereas the amount of glucose formed from lactate decreased from 2.0 +/- 0.1 to 1.4 +/- 0.2 mumol.kg-1.min-1 (P less than 0.02) and the percent of lactate turnover converted to glucose decreased from 26 +/- 1 to 20 +/- 2% (P less than 0.05). We conclude that insulin inhibits overnight glucose Ra from lactate by decreasing the proportion of lactate diverted towards gluconeogenesis rather than by altering lactate availability or total flux.

Adult↗
PubMed1985

Effect of lactation on cholesterol synthesis in rats.

Lactation induces a variety of morphological and functional changes in the gastrointestinal tract. In the present study we employed tritiated water as the substrate to demonstrate that in the intact rat lactation results in a twofold increase in cholesterol synthesis in the small intestine. Feeding a high-cholesterol diet did not markedly inhibit small intestinal cholesterol synthesis in either control or lactating animals, and the difference in cholesterol synthesis between the two groups persisted. In the large intestine, cholesterol synthesis is increased threefold in the lactating animals, and feeding a high-cholesterol diet did not affect synthesis in either the control or lactating animals. In the liver, lactation stimulated cholesterol synthesis, and quantitatively this increase in hepatic cholesterol synthesis is much greater than the increase observed in the intestines. Feeding the rats a high-cholesterol diet markedly inhibited hepatic cholesterol synthesis in both control and lactating animals, a finding that demonstrates that the feedback inhibition of cholesterol synthesis in the liver is not impaired by lactation. In the lactating animals, the quantity of labeled cholesterol in 1 ml of serum is 2.4 times greater than observed in controls. Feeding the rats a high-cholesterol diet markedly decreased the quantity of labeled cholesterol in the serum in both groups and obliterated the difference between control and lactating animals. This suggests that the increased hepatic cholesterol synthesis in the lactating animals is responsible for the differences in labeled cholesterol in the serum. Cholesterol feeding also reduced the quantity of labeled cholesterol localized to the mammary glands in lactating animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Pyruvate and lactate metabolism in the in vivo dog heart.

Pyruvate increases the phosphorylation potential in perfused heart to a greater extent than the closely correlated substrate L-lactate. Therefore, metabolism of these compounds was studied in the myocardium of intact dogs. Phosphocreatine/ATP was increased 23% at 5.3 mM plasma pyruvate but was not significantly increased by lactate except at the highest concentration (17.5 mM in blood). Calculated [ADP] fell during pyruvate infusion from 51.5 +/- 2.0 to 38.6 +/- 3.3 microM but did not change significantly during lactate infusion. Intracellular free [Mg2+] fell from 705 +/- 53 to 498 +/- 30 microM at the highest pyruvate infusion and from 692 +/- 112 to 417 +/- 19 microM with lactate infusion. Extraction of both substrates was linear at low concentrations, reaching 0.56 mumol lactate.min-1.g wet wt-1 at 17.5 mM blood lactate and 0.58 mumol pyruvate.min-1.g wet wt-1 at 5.3 mM plasma pyruvate. Therefore, lactate uptake was almost five times lower than pyruvate uptake at similar concentrations. Elevated pyruvate (> 3 mM) resulted in almost complete inhibition of net lactate uptake. Infused [3-13C]lactate or -pyruvate gave rise to labeled glutamate and alanine in vivo, but labeled lactate was not visible when [3-13C]pyruvate was the substrate. The 13C enrichment of myocardial lactate was similar to alanine and acetyl CoA with infused [3-13C]lactate but was only one-half that of alanine and acetyl CoA when [3-13C]-pyruvate was the substrate, indicating a possible inhibition of lactate dehydrogenase.

Animals↗
PubMed1995

Cerebral lactate metabolism in near-term fetal sheep.

The present study was designed to see if lactate can cross the blood-brain barrier of the near-term fetal sheep and replace glucose as an oxidative substrate during normoglycemia and acute insulin-induced hypoglycemia. Cerebral uptake of glucose, oxygen, lactate, and [14C]lactate as well as cerebral production of 14CO2 were measured under three conditions: 1) normoglycemia-normolactemia, 2) acute hypoglycemia-normolactemia, and 3) hypoglycemia-steady-state hyperlactemia. Although uptake of tracer [14C]lactate was consistent, there was no net uptake of unlabeled lactate during either normoglycemia or hypoglycemia. When arterial lactate concentration was raised from 2.2 +/- 0.5 to 3.3 +/- 0.4 (SE) mM by sodium lactate infusion, however, lactate was taken up. Comparison of cerebral [14C]lactate uptake with 14CO2 production indicated that the principal metabolic fate of lactate is oxidation. At increased concentrations, exogenous lactate accounted for approximately 7% of cerebral oxygen consumption. This study demonstrates that lactate crosses the blood-brain barrier of the near-term fetal sheep, is oxidized, and at elevated concentrations can partially replace glucose as an oxidative substrate during acute hypoglycemia.

Animals↗