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PubMed1988

Lactate production and release in cultured astrocytes.

Intracellular lactate content and release of lactate into the surrounding medium of mouse astrocytes in primary culture was measured using the lactate dehydrogenase method. During culturing the cellular content of astrocytes decreased from 400 to 200 nmol/mg protein. The total lactate released into the extracellular space, however, amounted to 75,000 nmol/mg within 98 h, corresponding to a lactate concentration of 10 mM in the cell culture dish. In another set of experiments, cytotoxic swelling was evoked by exposure of the cells to 60 mM K+, this situation caused a 40% increase in cellular volume and an increase in the KCl content of astrocytes. Within 3 h of a change to 60 mM K+ the intracellular lactate content was increased by 100 nmol/mg (one third) and the lactate release in the extracellular space by about 2000 nmol/mg (twice as high as during exposure to 3 mM K+). However, due to the increased intracellular water content, the lactate concentration inside the cells remained unchanged. It is concluded that astrocytes produce substantial amounts of additional lactate during cytotoxic swelling. This lactate, however, is not increasing the intracellular osmolarity and most of the lactate is released into the extracellular space. Depending on the transmembrane transport mechanism it could have the capability to decrease the strong ion difference and contribute to acid shifts in the extracellular space.

Animals↗

PubMed2001

Lactation failure in crossbred Sahiwal Friesian cattle.

Milk producers in Malaysia make extensive use of crossbred Sahiwal Friesian dairy cattle. These animals have, however, been found susceptible to lactation failure. A survey of cows in an experimental herd of F1 Sahiwal Friesian animals indicated that, in 30% of animals, milk yield decreased to negligible levels within the first 8 weeks post partum. Lactation failure was associated with a progressive increase in the amount of residual milk left in the udder after normal milking. By week 3 of lactation, residual milk volume was significantly greater than that in animals that, based on previous lactation history were not susceptible to lactation failure, and accounted for up to 30% of milk available at the morning milking. The cellular consequences of residual milk accumulation were evident in the activities of acetyl-CoA carboxylase, fatty acid synthetase and galactosyltransferase, key enzyme markers of cellular differentiation, which decreased in glands undergoing lactation failure and were lower than values measured in tissue of control cows. Mammary cell number, estimated by tissue DNA content, was also reduced in animals undergoing lactation failure. These indices of mammary development indicate that lactation failure is the result of premature involution in susceptible animals. Premature involution is a predictable consequence of progressive milk stasis in failing lactation, and attributable to an increase in autocrine feedback by inhibitory milk constituents. The progressive increase in residual milk is, on the other hand, unlikely to be attributable to impaired mammary development. Measurements of milk storage during milk accumulation showed no differences between control and lactation failure cows in the distribution of milk between alveolar and cisternal storage compartments. We conclude that lactation failure in Sahiwal Friesian cows is due to a failure of milk removal, and probably the result of an impaired milk ejection reflex rather than to the glands' milk storage characteristics.

Animals↗

PubMed1991

Effect of endurance swimming on the lactate kinetics of rainbow trout.

The lactate turnover rate of rainbow trout (Oncorhynchus mykiss) was measured by bolus injection of [U-14C]lactate at rest and during prolonged swimming at 85% Ucrit to determine the importance of this metabolic fuel for endurance locomotion in fish, to assess whether lactate exchange between white and red muscle could be a possible mechanism for supplying oxidizable fuel to their lateral red muscle, and to compare the contribution of lactate to total energy provision between teleost and mammalian species. Turnover rate only increased from 4.41 +/- 0.33 to 9.71 +/- 1.69 mumol kg-1 min-1 between rest and prolonged swimming, and the contribution of lactate oxidation to total metabolism declined during exercise. Lactate exchange between white and red muscle is, therefore, not a significant mechanism to fuel the active lateral red musculature during prolonged swimming. The lactate turnover rate of teleosts is one or two orders of magnitude lower than in mammals of equivalent size, but lactate has the same importance as a fuel in both vertebrate groups. However, lactate turnover rate and oxidation rate do not scale with body mass in the same fashion as does metabolic rate. The slope of the mammalian relationship for whole-body lactate turnover and oxidation is much lower (0.58) than the slope of the classic relationship for metabolic rate (0.75), indicating that lactate is a much more important oxidative substrate for small than for large animals.

Animals↗

PubMed1976

Effect of lipids on the reconstitution of D-lactate oxidase in Escherichia coli membrane vesicles.

An unsaturated fatty acid auxotroph lacking D-lactate dehydrogenase activity has been isolated from Escherichia coli ML 308-225 dld-3. While NADH oxidase activity in membrane vesicles prepared from the mutant cells grown in a variety of unsaturated fatty acids is comparable to that of previously isolated fatty acid auxotrophs, D-lactate oxidase activity is absent. However, D-lactate oxidase ativity can be restored when vesicles are incubated with a purified preparation of D-lactate dehydrogenase obtained from wild type cells. The effect of altering the fatty acid composition of the membrane on the reconstitution of D-lactate oxidase activity was examined. Binding of purified D-lactate dehydrogenase was not affected by either the lipid composition of the membrane vesicles or the temperature during reconstitution. However, the reconstitution of D-lactate oxidase activity was strongly influenced by the fatty acid composition of the membrane lipids. The temperature dependence of the reconstituted activity was analyzed. Temperature transitions were not observed with membrane vesicles supplemented with oleic or linolenic acid but palmitelaidic acid-enriched vesicles exhibited a transition temperature at 30 degrees. Attempts to reconstitute the elaidic-supplemented vesicles at temperatures below 30 degrees failed to yield active D-lactate oxidase and the vesicles aggregated. At 42 degrees, aggregation did not occur and D-lactate oxidase activity was obtained to a level of 10% of that found with membranes from the parent strain (ML 308-225). These results suggest that although binding of D-lactate dehydrogenase is independent of the physical state of the membrane, reconstitution of the D-lactate oxidase activity in membrane vesicles is dependent upon the fatty acid composition of the phospholipid, hence the physical state of the membrane.

Cell Membrane↗

PubMed1990

Whole population cell kinetics of jejunal and colonic epithelium in lactating dams.

Previous studies make it likely that the response of the intestinal epithelium as a whole to lactation is different from that observed in the crypt population alone. We confirm this difference by whole population cell kinetics measurements of jejunal and colonic epithelium in mice that have been suckling pups for various lengths of time. We found that the fraction of cells in S phase in jejunal epithelium was significantly increased after only 1 week of lactation, maintained this elevated level after 2 weeks of lactation, but returned to normal during the third week of lactation. The cell number density in jejunum was also significantly higher after 2 and 3 weeks of lactation before returning to normal by 4 weeks. In the colonic epithelium no changes were found in the distribution of cells in G1, S, and G2 + M phases. However, a significant increase in cell number density was observed after 2 weeks of lactation, followed by a sharp decrease to a level significantly below that of normal mice after 3 and 4 weeks of lactation. We conclude that the observed significant increase in the fraction of S phase in jejunal epithelium of lactating mice is probably due to a smaller relative expansion of the villus population when compared with the expansion of the crypt population. Our data also indicate that a number of cell kinetic parameters in the intestinal epithelium of lactating mice are changing throughout the period of lactation. Thus the intestinal epithelium is probably not in a steady state during lactation.

Animals↗

PubMed1998

Safety assessment of lactate esters.

Lactate esters have an oral LD50 greater than 2000 mg/kg and the inhalation LC50 is generally above 5000 mg/m3 and they may be potential eye and skin irritants, but not skin sensitizers. No evidence of teratogenicity or maternal toxicity was observed in an inhalation (2-ethylhexyl-l-lactate) or dermal study (ethyl-l-lactate). Subacute inhalation studies have been conducted at concentration up to 600 mg/m3 or higher on four lactate esters (ethyl, n-butyl, isobutyl, and 2-ethylhexyl-l-lactate). Degenerative and regenerative changes in the nasal cavity were noted in all studies. The NOAEL in ethyl, n-butyl, and isobutyl-l-lactate vapor studies was 200 mg/m3. For aerosol exposure, 2-ethylhexyl-l-lactate, the most toxic of the lactates, minimal damage to the nasal epithelium was noted at 75 mg/m3 with vapor being slightly less toxic than the aerosol. Lactates do not appear to cause systemic toxicity, except at very high concentrations (1800 mg/m3 or higher). These systemic effects may be secondary to severe irritation seen at high doses. Sensory irritation tests suggest that a vapor exposure limit of 75 mg/m3 ( approximately 15 ppm) should prevent irritation in humans and therefore an occupational exposure level for vapor of 75 mg/m3 is recommended. However, aerosol exposure should be kept as low as possible. The low vapor pressure of the higher molecular weight esters would tend to keep vapor exposure low and the odor of lactate esters serves as a warning of exposure. These lactate esters are readily biodegradable, suggesting little concern from an environmental point of view.

Administration, Inhalation↗

PubMed1994

Continuous monitoring of lactate during exercise in humans using subcutaneous and transcutaneous microdialysis.

We have evaluated the possibility of monitoring the plasma lactate concentration in human volunteers during cycle ergometer exercise using subcutaneous and transcutaneous microdialysis. In transcutaneous microdialysis, the relative increase in dialysate lactate concentration exceeded that of plasma lactate concentration by a factor of 6 during exercise due to exercise-induced lactate secretion in sweat. During exercise the subcutaneous microdialysis dialysate lactate concentration underestimated the plasma lactate concentration possibly due to diffusion limitation or adipose tissue lactate production. While it was demonstrated that microdialysis can be used for on-line lactate monitoring, neither subcutaneous nor transcutaneous dialysate lactate concentration were linearly related to the plasma lactate concentration during exercise, and it was found therefore that it was not possible to monitor directly plasma lactate concentration during exercise.

Adult↗

PubMed1987

Blood lactate parameters related to aerobic capacity and endurance performance.

The relationships among four descriptors of lactate increase: lactate threshold (LT) (the VO2 at which blood lactate concentration begins to increase above the resting level during an incremental exercise test), LT1 (the VO2 at which blood lactate increases 1 mM above the resting level), LT2 (the VO2 at which blood lactate concentration reaches a fixed value of 2 mM), onset of blood lactate accumulation (OBLA; the VO2 at which blood lactate reaches a concentration of 4 mM), were compared with aerobic capacity (VO2max) and 12 min running performance in 19 untrained female students. The VO2 (+/- SD) of LT, LT1, LT2, OBLA, and VO2max were 14.5 +/- 3.7 ml X kg-1 X min-1, 22.5 +/- 4.3 ml X kg-1 X min-1, 22.2 +/- 4.5 ml X kg-1 X min-1, 30.3 +/- 5.2 ml X kg-1 X min-1 and 36.0 +/- 5.1 ml X kg-1 X min-1, respectively. The mean (+/- SD) distance covered in the 12 min running was 2356 +/- 160 m. The results were as follows: 1) the lactate parameters (i.e. LT, LT1, LT2, and OBLA) were highly correlated with each other. 2) all the lactate parameters were related to VO2max and endurance running performance with a high correlation coefficient. Of the four descriptors of lactate change with exercise, LT correlated best with VO2max and endurance running performance compared to LT1, LT2 and OBLA. It is concluded that lactate threshold is the best index for aerobic capacity and endurance running performance.

Adult↗

PubMed1990

Lactate transport and glycolytic activity in the freshly isolated rabbit cornea.

Studies on the intact avascular cornea reveal two types of lactate effluxes: exogenous glucose-elicited and spontaneous. The former type exhibits characteristics resembling the proton-lactate symport system previously found in tumor cells and erythrocytes, including an enhanced lactate efflux at a higher extracellular pH and in the presence of H+ and K+ ionophores, and an inhibition by mersalyl with subsequent lactate accumulation in the tissue and cessation of glycolytic activity. The latter type occurs immediately following the incubation of freshly isolated cornea in a medium containing no exogenous glucose, with a rate about 10 times that of exogenous glucose-elicited lactate efflux. It is insensitive to 10 mM iodoacetate and lacks the characteristics of the proton-lactate symport system. Findings reveal that about 50% of corneal glucose utilization occurs in the epithelium, with the stroma and endothelium sharing the other 50% approximately equally. Of the glucose utilized, the lactate formation to pyruvate oxidation rate ratios are approximately 1:1 in the epithelium, 2:1 in the stroma, and 1:2 in the endothelium. About 79% of total tissue lactate is formed in the epithelium and stroma, and in vivo, this is probably pumped into the stromal extracellular space (about 90% of total tissue volume) via the proton-lactate symport system, with spontaneous release into the aqueous humor via a simple diffusion process. The H+ and K+ ionophores facilitate lactate efflux at the expense of the cellular pyruvate pool, without significant effect on the glucose uptake and glycolytic activity. These findings suggest that the ionophore-mediated lactate efflux favors the reduction of low pyruvate concentration in the tissue, rather than parallel increases in glycolytic activity.

3-O-Methylglucose↗

PubMed1988

L(+)-lactate transport in perfused rat skeletal muscle: kinetic characteristics and sensitivity to pH and transport inhibitors.

We have examined lactate uptake (as the rate of net muscle lactate accumulation) and unidirectional inward transport (measured by a paired-tracer dilution method) in muscle of the perfused skinned rat hindlimb. Inhibition of tracer influx (fractional uptake at 1 mM L(+)-lactate, 43.3 +/- 3.1% but only 32.9 +/- 1.8% at 50 mM lactate) suggested some competition between tracer and native forms of the carboxylate for transport. D(-)-lactate (50 mM) did not inhibit uptake of tracer L(+)-lactate. Pyruvate (25 mM), but none of five other monocarboxylates, inhibited uptake of tracer lactate, by 22% (P less than 0.01). Altering perfusate pH from 7.4 to 6.8 caused a 36% increase (P less than 0.001) in the unidirectional L(+)-lactate transport at 1 mM L(+)-lactate, whereas increasing pH to 7.7 reduced transport by 18% (P less than 0.01). Tracer lactate influx was inhibited by 500 microM 4-acetamido-4'-isothiocyanostilbene (SITS) (19%), 5 mM alpha-cyano-4-hydroxycinnamic acid (CIN) (20-30%), 1 mM amiloride (27%) and by a thiol group reagent p-chloromercuribenzenesulphonic acid (pCMBS) (26%). Overall the results indicate that at least two processes are involved in the transfer of lactate: one, saturable, with a Vmax of 0.84 mumol.min-1.g-1 and an apparent Km of 21 mM was sensitive to SITS, CIN, and a thiol group reagent; the other was non-saturable and insensitive to SITS and CIN with an apparent rate constant of 0.1 min-1.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed1996

Noradrenergic facilitation of the adrenocorticotropin response to stress is absent during lactation in the rat.

During lactation, the regulation of the activity of the hypothalamic-pituitary-adrenal (HPA) axis is modified in that tonically elevated glucocorticoid secretion is observed together with blunted ACTH secretion following exposure to various stressors. Although decreased CRF mRNA levels have been reported in neurons of the paraventricular nucleus (PVN) which control ACTH secretion, the mechanisms underlying stress hyporesponsiveness during lactation are still largely unknown. In addition, lactation is associated with inhibition of reproductive functions and the involvement of the PVN neurons in this inhibition is unclear. In these studies, we tested the hypothesis that the effects of stimulatory noradrenergic afferents to the hypothalamic PVN are decreased during lactation, maintaining stress hyporesponsiveness. We also determined whether PVN noradrenergic afferents could modulate suckling-induced luteinizing hormone (LH) suppression. Virgin and lactating females, on day 2 of lactation, received either sham (SHAM) or 6-hydroxydopamine (6OH-DA) lesions over the PVN. Suppression of plasma LH secretion following a suckling test was determined on day 9 in ovariectomized females and plasma ACTH and corticosterone (B) responses to swim stress were determined on day 11 of lactation. In virgin females, 6OH-DA lesion caused a significant reduction in the ACTH and B responses to swim stress. In SHAM lactating females, plasma ACTH response to stress was blunted compared to SHAM virgins, but 6-OHDA lesion did not reduce ACTH levels further. Lesions in lactating females reduced basal LH secretion, although not significantly, but suckling did not further inhibit LH secretion as observed in SHAM lactating females. In all lesioned groups, PVN tyrosine hydroxylase (TH) immunoreactivity was reduced compared to SHAM rats. These results suggest that brainstem (nor)adrenergic inputs to the PVN act to facilitate ACTH stress response in virgin rats, while in lactating rats this facilitation is absent. In addition, (nor)adrenergic cells projecting to the PVN might also participate in the modulation of GnRH and LH secretion during suckling.

Adrenocorticotropic Hormone↗

PubMed1986

The effect of lactate on acetylcholine release evoked by various stimuli from Torpedo synaptosomes.

The effect of external lactate on acetylcholine (ACh) release was examined at the nerve electroplaque junction of Torpedo marmorata using cholinergic synaptosomes prepared from the electric organ. Lactate reduced the release of ACh triggered by depolarization of synaptosomes with potassium. However, the release mechanism itself was not affected by lactate since, in its presence, the ACh release induced by different agents such as the calcium ionophore, A23187, or gramicidin D was equal to the release by control synaptosomes (without lactate). A possible site of action for lactate would be the voltage-dependent Ca2+ influx mediated by the natural calcium channel which is thought to couple depolarization and release and which would be bypassed during ionophore-induced Ca2+ entry. An intracellular target was indicated because decreasing the extracellular pH made L(+)lactate a slightly more potent inhibitor. The involvement of a membrane transporter for lactate was suggested by the observation that the D(-) isomer of lactate was less potent than the natural L(+) isomer. The release of endogenous lactate by electric organ prisms was also determined and depolarization with high potassium strongly stimulated L(+)lactate release from prisms. These results suggest that lactate production by stimulated postsynaptic electroplaques may inhibit acetylcholine release from presynaptic nerve terminals, constituting an example of negative feedback.

Acetylcholine↗

PubMed1981

Disturbances of lactate metabolism in patients with liver damage due to paracetamol overdose.

Six patients with liver damage following paracetamol overdose, one patient with viral hepatitis and six control subjects were infused with sodium L(+) lactate. In controls the results were analysed using a single compartment model while in paracetamol patients a two compartment system was used to derive the fractional rate removal constant and lactate distribution volume. Forearm arterio-venous differences of lactate were also determined in order to assess the role of voluntary muscle in removal of a lactate load. In paracetamol patients with fractional rate removal constant was decreased to less than half the control value (P less than 0.001) while total distribution volume was similar to the two groups. Fasting lactate concentrations were significantly increased in paracetamol patients due to diminished lactate removal since the endogenous production rate of lactate was not significantly different from controls. A greater proportion of the lactate load was removed in voluntary muscle in paracetamol patients (39%) than controls (17%). Since the balance of lactate removal occurs principally in the liver, the decrease in the fractional rate removal constant in patients following paracetamol overdose indicates a severe derangement of hepatic lactate metabolism with a compensatory increase in lactate metabolism in voluntary muscle.

Acetaminophen↗

PubMed1993

The effects of lactate loading on alanine and glucose metabolism in the conscious dog.

The effect of lactate per se on alanine and glucose metabolism was studied in five overnight-fasted conscious dogs. Somatostatin was infused to inhibit endogenous pancreatic insulin and glucagon release and the hormones were replaced intraportally at basal rates. Saline (n = 5) or lactate (at 25 and 50 mumol.kg-1.min-1 for 90 minutes each) was infused, and blood samples were taken during the last 30 minutes of each 90-minute period. Insulin, epinephrine, norepinephrine, and cortisol levels remained unchanged during saline or lactate infusion. Glucagon level decreased slightly during lactate (94 +/- 7 to 74 +/- 9 and 79 +/- 8 pg/mL) and saline (91 +/- 8 to 90 +/- 4 and 81 +/- 11 pg/mL) infusions. There were no significant changes in lactate or alanine levels or net hepatic balances with saline infusion. Blood lactate level increased from 657 +/- 74 to 1,718 +/- 126 and 3,300 +/- 321 mumol/L (both P < .05) during the low- and high-lactate infusion periods, respectively. The liver produced lactate during the control (5.57 +/- 2.92 mumol.kg-1 x min-1) and low-lactate infusion (1.75 +/- 2.58 mumol.kg-1 x min-1) periods, but consumed lactate (3.89 +/- 3.31 mumol.kg-1 x min -1; P < .05) during the high-lactate infusion period.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗

PubMed1995

Bone mineral loss during lactation and recovery after weaning.

OBJECTIVE: To test the hypothesis that bone mineral content (BMC) and density (BMD) are lost during lactation and regained within 6 months after weaning. METHODS: Two cohorts of women, defined by time postpartum, were enrolled into the study; each cohort was followed for 6 months. Women in the lactation cohort (65 lactating women and 48 nonlactating postpartum controls) were enrolled at 2 weeks postpartum. Women in the weaning cohort (40 lactating and 43 nonlactating postpartum controls) were enrolled at 4-6 months postpartum. Lactating women enrolled in the weaning cohort had been fully breast-feeding at enrollment and weaned within 2 months of enrollment. Bone mineral content of the total body and BMD of the lumbar spine and distal radius were measured by dual-energy x-ray absorptiometry. RESULTS: Lactating women lost significantly more bone in the total body (-2.8 versus -1.7%) and lumbar spine (-3.9 versus 1.5%) than did nonlactating women during the first 6 months postpartum. There was no effect of lactation on bone changes at the distal radius. After weaning, lactating women gained significantly more bone in the lumbar spine than did nonlactating women (5.5 versus 1.8%). Earlier resumption of menses was associated with a smaller loss of bone during lactation and a greater increase of bone after weaning. CONCLUSION: Women lose bone during lactation but gain bone after weaning. Thus, lactation may not result in net bone loss.

Adult↗

PubMed1988

Lactate utilization and influx in resting and working rat red muscle.

1. The behavior of lactate was studied during electrical stimulation and influx was measured under resting conditions of rat soleus muscle. 2. Lactate utilization was measured with (U-14C) lactate and results from electrical stimulation of the soleus muscle present evidence that this substance is mainly oxidized. 3. Under resting conditions, lactate influx showed a saturable transport system with an apparent Km of 11 mM. This low affinity for lactate suggests that lactate transport has a limiting factor for the muscle. 4. The increased lactate utilization under electrical stimulation (1,114 +/- 344 mumol/g/hr, at 20 mM lactate) corresponds to increased lactate permeability as compared to the influx rate (20.81 +/- 1.65 mumol/g/hr at 20 mM lactate) in resting conditions. 5. Alanine, epinephrine or S.I.T.S. 4-amino-4'isothiocyanostilbene-2-2'-disulphonate) do not affect lactate permeability in the soleus muscle.

Animals↗

PubMed1978

Mediated transport and metabolism of lactate in rat aorta.

1. Under appropriate conditions L- and D-lactate enter the cells of rat aorta and are metabolized. Oxidation of lactate to CO2 occurs under aerobic conditions. 2. L- and D-lactate are taken up into the cells when oxygen, glucose, or both oxygen and glucose are present in the incubation medium. Both L- and D-lactate are excluded from the cells when neither oxygen nor glucose is present. 3. D,L-Glyceraldehyde prevents the uptake of L-lactate. The effect is apparently not due to the inhibition of glucose metabolism by L-glyceraldehyde. 4. L-lactate (20 mM) markedly inhibits the uptake of 5 mM D-lactate, but 20 mM D-lactate fails to inhibit the uptake of 5 mM L-lactate. 5. Raising the pH of the incubation medium markedly depresses the uptake of L-lactate. 6. The results provide evidence that L- and D-lactate enter the cells of rat aorta by a mediated transport system.

Animals↗

PubMed2005

Pregnancy increases plasma leptin in nulliparous but not primiparous goats while lactation depresses it.

Most dairy ruminants are still lactating during early pregnancy, which could induce hormonal adaptations different from those observed during pregnancy alone. The incidence of concomitant lactation and pregnancy on plasma leptin has not been studied, and physiological factors involved in its regulation have not been addressed in goats. We assayed leptinemia throughout the pregnancy-lactation cycle in nulliparous and primiparous goats, starting 165 days prior to parturition and finishing 59 days after. During the first half of pregnancy, primiparous goats were lactating. Lactating non-pregnant primiparous goats were studied in parallel. Plasma leptin increased (+49%) up to mid-pregnancy in nulliparous, but not in primiparous goats. Furthermore, leptinemia was similar between pregnant and non-pregnant lactating primiparous goats, suggesting a strong leptinemia down-regulation by late lactation. Plasma leptin decreased from mid-pregnancy to parturition, more markedly in nulliparous goats, and remained depressed during early lactation at a similar level in both female types. It was lower, at 130 days of pregnancy, in goats carrying two fetuses. The leptinemia down-regulation by late pregnancy was highlighted by the lack of plasma leptin increase after drying-off late-pregnant primiparous goats, while it strongly increased in non-pregnant goats. The observation of leptinemia increase only in nulliparous goats suggests that it is not an essential endocrine adaptation during early pregnancy. By contrast, in both female types, the low leptinemia during transition from late pregnancy to lactation, and during late lactation, may be important for the adaptations that occur during lactation such as the partitioning of energy and nutrients towards essential functions and/or hyperphagia.

Animals↗