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Inhibition of endogenous oxalate production: biochemical considerations of the roles of glycollate oxidase and lactate dehydrogenase.

1. Both the peroxisomal, flavin-linked glycollate oxidase [(S)-2-hydroxy-acid oxidase; EC 1.1.3.15] and the cytosolic, nicotinamide-adenine dinucleotide (NAD)-linked lactate dehydrogenase (L-lactate dehydrogenase; EC 1.1.1.27) are thought to contribute to the formation of oxalate from its immediate precursors, glycollate and glyoxylate, but the relative contributions of each enzyme to endogenous oxalate production is not known. 2. In rat liver homogenates, [14C]oxalate production from labelled glycollate is halved and that from labelled glyoxylate is increased fourfold by the addition of either NAD or NADH. 3. In isolated rat hepatocytes, the 3-hydroxy-1H-pyrrole-2,5-dione derivatives of glycollate, which are specific inhibitors of glycollate oxidase, have a greater effect on glycollate metabolism than on glyoxylate metabolism. 4. These findings are consistent with an important role for lactate dehydrogenase in oxalate formation from glyoxylate. 5. With human and rat liver homogenates and with purified human liver glycollate oxidase and rabbit muscle lactate dehydrogenase, DL-phenyl-lactate (2 mmol/l) completely inhibits glycollate oxidase but has not effect on lactate dehydrogenase. On the other hand, the reduced form of a chemically synthesized, NAD-pyruvate adduct (1 mmol/l) almost completely inhibited lactate dehydrogenase but had no effect on glycollate oxidase. 6. Either alone or in combination, DL-phenyl-lactate and reduced NAD-pyruvate adduct reduce oxalate production from glycollate and glyoxylate in isolated rat hepatocytes, but do not abolish it completely. 7. These findings support a role for another enzyme, probably glycollate dehydrogenase (EC 1.1.99.14), in oxalate production in integrated cell metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Oxidoreductases↗

Suckling-induced Fos-immunoreactivity in subgroups of hypothalamic POMC neurons of the lactating rat: investigation of a role for prolactin.

Attention has recently been focused on lactation-induced modifications of activity of neuronal populations in the arcuate nucleus (ARC) of the mediobasal hypothalamus. The ARC hosts the tubero-infundibular dopaminergic (TIDA system) responsible for the neuroendocrine control of prolactin (PRL), and other non-neuroendocrine neuronal populations, such as neuropeptide Y (NPY)- and proopiomelanocortin (POMC)-containing systems that are important modulators of hypothalamic gonadoliberin (GnRH) secretion. Our longstanding interest in the functional anatomy of the ARC led us to investigate whether the suckling stimulus would trigger an expression of Fos-ir in specific arcuate neuronal populations and to possibly characterize responsive neurons by using double-labeling immunohistochemistry. Freely nursing lactating females expressed strong Fos-ir in neurons of the ARC compared to diestrous females. Fos-ir was encountered in neurons not belonging to the TIDA system and that was for a large proportion identical to the POMCergic neurons. We showed that, in lactating females submitted to suppression of the suckling stimulus by removal of the pups, the pattern of expression of Fos-ir is similar to that seen in diestrous females and that, a pattern of expression of Fos-ir indistinguishable from that observed during free lactation is reinstated a short time after the return of the pups and restoration of the suckling stimulus, suggesting that this expression of Fos-ir strictly depends upon the presence of the newborns and the suckling stimulus. By lowering circulating levels of the PRL with bromocryptine-or PRL antiserum-treatment, we noticed a decrease in the number of (beta-endorphin + Fos)-ir neurons compared to non-injected freely nursing lactating females. By maintaining high levels of circulating PRL with haloperidol-treatment, we observed a number of colocalizations close to that observed in freely nursing lactating females. Our results suggest that during lactation a rostral subgroup of the arcuate POMCergic neuronal population is activated at least partially in response to the suckling-induced secretion of PRL and that this activation participates in maintaining the endocrine and/or metabolic demands of the lactational status.

Animals↗

Endocrine bases of lactational anoestrus in the sow.

Parturition in the sow is followed by a period of anovulation which is prolonged by lactation. Follicular development and luteinizing hormone (LH) secretion are depressed during the last month of pregnancy. After parturition, LH secretion increases but is again inhibited by the establishment of lactation. Lactating sows are submitted to stimuli originating from the young, whose intensity culminates 3-14 d post-partum (pp), and to high nutrient requirements for milk production. The inhibitory effects of sucklings are imposed during the first 3 d pp and seem to be mediated by the action of opioids at the hypothalamic level. The nutritional deficit constitutes an additional inhibitory factor. As lactation continues, LH secretion progressively increases. A further rise in LH occurs at weaning. Variations in follicle-stimulating hormone (FSH) profiles are less marked. The divergence observed between LH and FSH might be explained by different mechanisms of control; FSH secretion depends mainly on ovarian inhibition whereas LH secretion depends mainly on factors related to lactation. Folliculogenesis progressively resumes during lactation and follicles acquire the ability to respond to the weaning-associated stimuli and begin preovulatory growth. Hormones modified by lactation, such as prolactin, insulin, growth hormone and insulin-like growth factor I, may influence folliculogenesis directly at the ovarian level or via modifications of gonadotrophin secretions. In conclusion, the inhibition of the hypothalamo-pituitary-ovarian axis during lactation is mainly due to suckling-induced neuroendocrine reflexes. We hypothesize that the nutritional deficit becomes relatively more important during the third and fourth weeks pp.

Anestrus↗

Acidosis induced by lactate, pyruvate, or HCl increases blood viscosity.

PURPOSE: Serum lactate correlates with the severity of disease and the mortality in shock. It is not clear if lactate is only a marker or a mediator of disease. We tested the hypothesis that acidosis induced by lactate and pyruvate affects blood flow properties. MATERIALS AND METHODS: Human blood was incubated with additional lactate (0-50 mmol/L) or pyruvate (0-25 mmol/L) for 1 hour at 37 degrees C. Blood viscosity was measured at high (94.5 s(-1)) and low (0.1 s(-1)) shear rate. Hematocrit was measured with an electronic particle counter as well as centrifugation. RESULTS: A total of 50 mmol/L additional lactate produced acidosis (pH 6.4) and increased whole-blood viscosity at high shear rate (94.5 s(-1): 6.53 +/- 0.51 mPa.s vs 4.94 +/- 0.18 mPa.s for control, n = 5, P <.001) and low shear rate (0.1 s(-1): 93.9 +/- 18.6 mPa.s vs 53.5 +/- 7.7 mPa.s, n = 5, P <.001). Simultaneously, an increased centrifuged hematocrit was observed (about 7% with 50 mmol/L lactate, P <.001), indicating eryth-rocyte swelling. These changes were reversible on removal of lactate. The addition of 25 mmol/L pyruvate also induced acidosis and increased blood viscosity and centrifuged hematocrit. When HCl was used to induce a comparable pH level decrease, a similar increase in blood viscosity and hematocrit were observed. CONCLUSIONS: Pronounced acidosis induced by either lactate, pyruvate, or HCl impairs blood flow properties, which may contribute to the understanding of the pathophysiology of critical illness.

Acidosis↗

Relation between plasma lactate concentration and fat oxidation rates over a wide range of exercise intensities.

Increasing exercise intensities will induce an increase in glycolytic flux. High glycolytic activity is associated with reduced fat oxidation rates and increased accumulation of lactate. Both lactate and hydrogen ions have been shown to be directly related to the decreased fat oxidation rates. The aim of the present study was to determine whether the exercise intensity at which maximal fat oxidation rates occur coincides with the intensity at which lactate starts to accumulate in plasma. Thirty-three moderately trained endurance athletes performed a graded exercise test to exhaustion on a cycle-ergometer with 35 W increments every three minutes. Expired gas analysis was performed throughout the test and stoichiometric equations were used to calculate fat oxidation rates. The intensity which elicited maximal fat oxidation (Fat (max)) and the intensity at which fat oxidation rates became negligible (Fat (min)) were determined. Blood samples for lactate analysis were collected at the end of each stage of the graded exercise test. The intensity at which lactate concentration increased above baseline (LIAB) and the lactate threshold (LT-D) were determined (D-max method). Fat (max) was located at 63 +/- 9 % V.O (2)max and LIAB at 61 +/- 5 % V.O (2)max and there appeared to be no statistical difference between the two intensities. Fat (max) and LIAB were significantly correlated. Fat (min) and LT-D were also significantly correlated but were located at different intensities (82 +/- 7 and 87 +/- 9 % V.O (2)max respectively). The data of the present study showed that accumulation of lactate in plasma is strongly correlated to the reduction seen in fatty acid oxidation with increasing exercise intensities. The first rise of lactate concentration occurred at the same intensity as the intensity which elicited maximal fat oxidation rates.

Adult↗

Sweat lactate, ammonia, and urea in rugby players.

The purpose of this study was to investigate sweat lactate, ammonia, and urea excretion in rugby players. Fifteen elite amateur rugby players volunteered to participate. The study was conducted during competitive matches in the official season. Plasma and sweat concentrations of lactate, ammonia, and urea were measured before and after the matches. Peak values for creatine kinase activity were observed 24 h after the match. There was no significant change between time points for blood lactate concentration but secretion rate per unit surface and time was significantly reduced after the match. Sweat ammonia concentration increased significantly during the match; values were significantly reduced after 24 h and still remained low at 72 h. Secretion rate was also reduced from 24 h. Urea concentration was significantly reduced at 48 h, while secretion rates decreased at 24 h and 48 h. Lactate in blood was significantly elevated during the match but not thereafter. Blood ammonia was significantly elevated during the match and did not differ from the resting values at 24 or 48 h. Urea in blood tended to decrease during the match, with a significant reduction at 24 h. Significant positive correlations were observed between blood and sweat concentrations for urea and ammonia but not for lactate. Sweat rate correlated positively with sweat lactate secretion. The fact that part of the ammonia formed during exercise is lost with sweat indicates the importance of the purine nucleotide cycle during rugby matches. Our data also confirm that sweat lactate concentration is not influenced by circulatory blood lactate in rugby players.

Adult↗

Influence of lactate on isoproterenol-induced lipolysis and beta-adrenoceptors distribution in human fat cells.

The influence of lactate on human adipocytes lipolysis and the possible relationship between lactate-induced metabolic effects and beta-adrenoceptor binding sites were investigated. beta-sites were identified in membranes with (125I)-cyanopindolol and in intact cells with (125I)-cyanopindolol and (3H)-CGP 12177. Lactate reduced isoproterenol-induced lipolysis in a dose-response fashion and such inhibition became significant only at 16 mmol/l lactate. Exposure of human fat cells to 16 mmol/l lactate significantly reduced beta-adrenoceptors density on crude membranes. When the binding assay was performed on intact cells using (125I)-cyanopindolol at 37 degrees C, the radioligand identified the same number of receptors, regardless of the presence of lactate in the preincubation medium. When (3H)-CGP 12177 was used, it bound to about 35% less receptors in lactate pre-treated cells than in control. Seemingly, at 37 degrees C, because of its lipophilicity, (125I)-cyanopindolol can cross the plasma membrane and bind to intracellular sites whereas, (3H)-CGP 1277, due to its hydrophilicity, identifies surface receptors only. Thus, the present in vitro study provides evidence that high levels of lactate, similar to the concentrations usually achieved in overt lactic acidosis, are able per se to inhibit human lipolysis and to redistribute beta-adrenoceptors from cell surface to a domain not accessible to hydrophilic ligands.

Adipose Tissue↗

Metabolism and action of insulin and glucagon in goat during lactating and dry period.

The metabolism and action of insulin and glucagon were investigated in goats during mid lactating (50 days postpartum) and during the dry period. The animals were fed hay and concentrate during lactation (1:1) and only hay during dry period. Pulse doses of unlabelled insulin and glucagon were injected intravenously. The disappearance of insulin from the circulation was faster during lactation than during dry period; the metabolic clearance rate of insulin was significantly increased during lactation. In contrast, the kinetic parameters of glucagon disappearance were very similar during the two periods. Basal plasma hormones (i.e. before hormone injection) were higher during lactation than during dry period; the molar ratio insulin:glucagon was left unchanged. The increase in plasma insulin following glucagon-stimulated hyperglycaemia was similar during the two periods. The ability of insulin to elicit a decrease in blood glucose was markedly impaired during lactation when compared to dry period. In contrast the ability of glucagon to increase blood glucose was slightly improved during lactation. Those endocrine changes could be related to the effect of both lactation and diet.

Amino Acids↗

Antegrade versus retrograde crystalloid cardioplegia: perioperative assessment of cardiac energy metabolism by means of myocardial lactate measurement.

The effects of retrograde and antegrade delivery of cold St. Thomas' Hospital cardioplegia were evaluated and compared in 21 patients who underwent elective myocardial revascularization. The patients were randomly separated into two groups: the antegrade group (n = 10), and the retrograde group (n = 11). Cardiac energy metabolism was monitored by evaluation of arterial and coronary sinus (CS) lactate concentration. There was an increase of the CS lactate concentration during aortic cross-clamp period in both groups. After release of the aortic cross-clamp, there was an increase of the CS lactate concentration in the antegrade group, and a decrease of CS lactate in the retrograde group. Analysis of the patients operated with antegrade delivery of cardioplegia showed an increase of the CS lactate concentration in 9/10 patients after aortic cross-clamp release. In the retrograde group, in 8/11 patients the CS lactate concentration decreased immediately after aortic cross-clamp release. Whereas the differences in the CS lactate concentration were not significantly different, the lactate extaction immediately after aortic cross-clamp release was significantly higher for the retrograde group (p = 0.034). This can be related to a faster reconsolidation of mitochondrial oxidative phosphorylation in the retrograde group. For the other registered parameters, hemodynamic recovery of cardiac function, release of creatine kinase MB isoenzyme, and clinical outcome, there was no significant difference between the groups. Based on this study we conclude that retrograde delivery of a cold non-oxygenated cardioplegic solution results in a better preservation of myocardial energy reserve than antegrade delivery.

Adult↗

Distinctive effects of three different modes of exercise on oxygen uptake, heart rate and blood lactate and pyruvate.

We intended to investigate the effects of different modes of exercise on oxygen uptake (VO2), the heart rate and the levels of lactate and pyruvate in venous blood. For this, untrained male subjects performed three modes of exercise with a treadmill (TR), a bicycle ergometer (UP) and a supine leg ergometer (SU). The percentage of maximal oxygen uptake (% VO2max) and VO2/weight for TR were significantly higher than those for UP or SU at lactate levels of 2, 3 and 4 mmol/l. The heart rate was also higher for TR than for SU at these lactate levels. The correlations of blood lactate with % VO2max, VO2/weight and the heart rate were significant for TR and SU, but not for UP. Blood lactate levels were lower for TR than for SU or UP at 60, 70, 80% VO2max, whereas the values for UP were lower than those for SU only at 60% VO2max. Blood pyruvate levels were always lower for TR than for SU. The ratios of lactate/pyruvate differed for TR and SU only at 60% VO2max. For a given mode of exercise, blood lactate and the ratio of lactate/pyruvate increased with an increase in % VO2max, but those of pyruvate did not. These results reveal that the relationships between any two of lactate, pyruvate, VO2 and the heart rate are different at different modes of exercise, and that blood lactate depends on adaptation of muscles to a mode of exercise rather than on the quantity of muscles mobilized.

Adult↗

Lactate, oxygen uptake, and cycling performance in triathletes.

To assess the relationship of exercise test variables to each other and to bike race times in an ultra-distance triathlon, we studied 24 participants (14 men, 10 women) in the 1985 Hawaii Ironman Triathlon, using a graded, maximal cycle ergometer test with gas exchange and blood lactate (LA) measurements at each work load. Exercise test variables were oxygen uptake (VO2) and heart rate (HR) at the lactate and ventilatory thresholds. Lactate threshold (LT-1) was defined as the exercise intensity that elicited a 1 mM increase in blood lactate concentration above the value measured during the first work load for each subject. Variables were also examined at the lactate thresholds of 2 mM and 4 mM. Ventilatory thresholds (VT) were identified as the points at which the ventilatory equivalent of oxygen (VE/VO2) increased without a corresponding increase in the ventilatory equivalent of carbon dioxide (VE/VCO2). Mean peak oxygen uptake (peak VO2) for this sample of Ironman triathletes was 57.4 ml.kg-1.min-1. Cycle peak VO2 was inversely correlated, r = 0.68 (P less than 0.0002) with bike finish time. VO2 and HR as well as the respective percentages of maximum were higher at all lactate thresholds than at VT (P less than 0.0001). Therefore VT should not be used to identify a lactate threshold in ultra-endurance triathletes. VO2 values at the lactate and ventilatory thresholds were not highly related to bike finish time (r = -0.26 to -0.58). Fractional utilization of peak VO2 (% peak VO2), HR, and % peak HR at thresholds were not related to bike finish time (r = -0.01 to 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Lactate exchange and removal abilities in sickle cell trait carriers during and after incremental exercise.

Arterial blood lactate concentrations and pH were measured on seven black male sickle cell trait (SCT) carriers before, during and after incremental exhaustive bicycle exercise (25 W increments per minute) and compared with those of six control individuals of the same ethnic origin having a similar physical fitness level. The object of the experiment was to determine if SCT has an effect on lactate kinetics. At volitional exhaustion which was reached at a comparable overall mean absolute work rate for both groups, oxygen consumption expressed per kilogram body mass was significantly lower for the SCT carriers than for the control volunteers. Lactate concentrations were higher for the SCT carriers after the 150 W exercise step but differences reached statistical significance only at exhaustion. Concentrations were distinctly higher for the SCT group during the following 40 minutes of recovery. While there were no observable differences in blood pH between the SCT and control subjects during the exercise, this variable became significantly lower for the SCT than for the control group 8 minutes after the end of exercise. Lactate recovery curves were fitted by a biexponential time function where the two velocity constants inform on the body's overall ability to exchange and remove lactate. The ability to remove lactate was comparable for the two groups. The present results do not warrant drawing a definite conclusion on impairment of the ability to exchange lactate in the presence of SCT. However, SCT carriers are likely to produce more lactate than control subjects reaching exhaustion at similar mean absolute work rate during exhaustive incremental bicycle exercise.

Adult↗

Influence of caffeine on blood lactate response during incremental exercise.

To test the hypothesis that caffeine ingestion prior to exercise would delay the onset of blood lactate accumulation, eight male subjects were studied during incremental exercise to maximal work rates on a cycle ergometer under two conditions: 1 h after ingestion of 200 ml of either decaffeinated, calorie-free cola (control trial) or the same cola drink with 5 mg caffeine/kg body weight added (caffeine trial). Maximal exercise values for oxygen consumption (VO2 max), ventilation, heart rate, respiratory exchange ratio (R), work rate, and blood lactate were not affected by caffeine. Submaximal exercise VO2, ventilation, and R also were unaffected by caffeine. During the caffeine trial, submaximal exercise blood lactate was significantly higher and heart rate significantly lower than during the control trial (P less than 0.05). The lower exercise heart rate at the same VO2 resulted in a significantly greater O2 pulse during all submaximal exercise intensities for the caffeine trial (P less than 0.05). Data on R indicated that caffeine had no effect on substrate utilization during exercise. Data on exercise blood lactate response suggested that caffeine does not delay and may accelerate the onset of blood lactate accumulation during incremental exercise. When defined as either a "breakpoint," delta l mM (above resting lactate), or fixed level of 4 mM, the lactate threshold (LT) did not differ between caffeine and control trials. However, in using a 2 mM lactate level as a criterion, the LT during the caffeine trial (2.13 +/- 0.22 l X min-1) was significantly (P less than 0.05) lower than during the control trial (2.71 +/- 0.17 l X min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Comparative profiles of the hexose monophosphate dehydrogenases in rat tissues over the lactation cycle.

The mammary gland tissue hexose monophosphate dehydrogenase activities were low in virgin, pregnant and weaned rats, but increased at the onset of lactation. The muscle and liver glucose 6-phosphate dehydrogenase activity peaked at early and late lactation respectively. The liver 6-phosphogluconate dehydrogenase peaked in late pregnancy and remained elevated through lactation. The muscle 6-phosphogluconate dehydrogenase peaked at the onset of lactation. The adipose tissue hexose monophosphate dehydrogenases exhibited small changes during pregnancy and lactation. The spleen hexose monophosphate dehydrogenases did not respond to lactation An overshoot in both the liver and the adipose tissue hexose monophosphate dehydrogenases was observed on weaning. Serum glucose levels remained unchanged throughout pregnancy, lactation and weaning. Only liver glucose 6-phosphate dehydrogenase activity correlated with plasma insulin, which also correlated positively with food consumption. The results demonstrate that tissue-specific control of the hexose monophosphate dehydrogenases occurs in the female rat during its complete lactation cycle.

Adipose Tissue↗

Expression of slc5a8 in kidney and its role in Na(+)-coupled transport of lactate.

We report here on the expression of slc5a8 in kidney and its relevance to Na(+)-coupled reabsorption of lactate. slc5a8 is the murine ortholog of SLC5A8, a candidate tumor suppressor gene, which we recently cloned from human intestine and demonstrated its functional identity as a Na(+)-coupled transporter for short-chain fatty acids and lactate. The slc5a8 cDNA, cloned from mouse kidney, codes for a protein consisting of 611 amino acids. When expressed heterologously in mammalian cells or Xenopus oocytes, slc5a8 mediates Na(+)-coupled electrogenic transport of lactate/pyruvate as well as short-chain fatty acids (e.g. acetate, propionate, and butyrate). The Na+/fatty acid stoichiometry varies depending on the fatty acid substrate (2:1 for lactate and 4:1 for propionate). This phenomenon of variable Na+/substrate stoichiometry depending on the fatty acid substrate is also demonstrable with human SLC5A8. In situ hybridization with sagittal sections of mouse kidney demonstrates abundant expression of the transcripts in the cortex as well as the medulla. Brush border membrane vesicles prepared from rabbit kidney are able to transport lactate in a Na(+)-coupled manner. The transport process exhibits the overshoot phenomenon, indicating uphill lactate transport in response to the transmembrane Na+ gradient. The Na(+)-coupled lactate transport in these membrane vesicles is inhibitable by short-chain fatty acids. We conclude that slc5a8 is expressed abundantly in the kidney and that it plays a role in the active reabsorption of lactate. slc5a8 is the first transporter known to be expressed in mammalian kidney that has the ability to mediate the Na(+)-coupled reabsorption of lactate.

Animals↗

Performance of dairy cows offered isonitrogenous diets containing urea or fishmeal in early and in mid-lactation.

Sixteen Friesian cows were used in Expt 1 to measure the effect of substituting urea-N with fishmeal-N either in early lactation (Part 1) or in mid-lactation (Part 2). In Part 1 (days 15-84 of lactation) the major N constituent of the concentrate was urea (U), urea-N: fishmeal-N in the ratio 2:1 (UF) or 1:2 (FU), or fishmeal (F). In Part 2 (days 84-175 of lactation) only urea (UM) and fishmeal (FM) were used. Replacement of urea-N with fishmeal-N significantly (P less than 0.05) increased yield of milk protein both in early and in mid-lactation. At both stages of lactation the cows were, by calculation, in positive energy balance. In mid-lactation replacement of urea-N by fishmeal-N significantly depressed (P less than 0.001) the concentration of fat in milk. Blood urea concentration decreased with increasing fishmeal inclusion (P less than 0.05) from U to FU. In Expt 2 the diets used in Expt 1, Part 1, were offered at a maintenance level of feeding to non-pregnant, non-lactating heifers in a 4 X 4 Latin square design experiment. Digestibility of dry matter, organic matter and cell-wall constituents increased progressively (P less than 0.05) with the first two increments of fishmeal inclusion. A major effect of replacing urea-N with fishmeal-N was to increase digestible organic matter intake (DOMI) and differences in DOMI between treatments in Expt 1, Part 1, accounted for observed differences in performance.

Animals↗

Relations between plasma non-esterified fatty acid metabolism and body fat mobilization in primiparous lactating goats.

During early lactation ruminants can mobilize considerable amounts of body fat to maintain milk production. The aim of the present study was to evaluate the efficacy of tritiated water (TOH) and non-esterified fatty acid (NEFA) kinetics as means of monitoring adipose tissue fat mobilization in lactating goats. Body fat, as estimated by a two-pool model of TOH kinetics, and NEFA entry rate were measured in four primiparous goats at days 11, 37 and 72 post partum. Estimated body fat decreased by an average of 64 g/d between days 11 and 37 of lactation, tending to increase between days 37 and 72. Plasma NEFA concentrations and NEFA entry rate decreased as lactation advanced, being significantly lower at day 72 than at day 11 of lactation. Both plasma concentrations of NEFA and NEFA entry rate were negatively correlated with calculated energy balance. Plasma NEFA concentrations and NEFA entry rate at days 11 and 37 of lactation were positively related to average body fat losses over the subsequent stage of lactation. These results demonstrate that NEFA kinetics reflect fat mobilization in primiparous lactating goats, particularly during negative energy balance.

Adipose Tissue↗

Non-esterified fatty acid and glycerol kinetics and fatty acid re-esterification in goats during early lactation.

Non-esterified fatty acid (NEFA) and glycerol kinetics were studied in lactating goats to gain insight into the mechanisms by which animals in early lactation can initially mobilize and later replenish body fat reserves. Kinetic measurements were made at days 10, 38 and 76 post-partum in ten multiparous lactating does. Plasma NEFA concentrations and NEFA entry rate decreased as lactation advanced, being significantly higher at day 10 than at either days 38 or 76 of lactation. Both plasma NEFA concentrations and NEFA entry rate were negatively correlated with calculated energy balance. In contrast, glycerol entry rate was significantly higher at day 76 than at day 10 of lactation and was positively related to both calculated energy intake and energy balance. Apparent intracellular fatty acid re-esterification was lower at day 10 than at later stages of lactation and was positively related to calculated energy balance. It is suggested that during early lactation, substantial shifts in adipose tissue fat reserves can occur via altering rates of fatty acid re-esterification and de novo lipogenesis, without major changes in the rate of lipolysis.

Animals↗