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PubMed1996

Effect of lactate on hepatic insulin clearance in perfused rat liver.

The aim of our study was to investigate whether sodium lactate has any effect on hepatic insulin dynamics in perfused rat liver. Rat livers were perfused in situ with saline or increasing concentrations of sodium lactate, and hepatic insulin extraction was calculated from the difference in insulin concentration between the portal and the suprahepatic vein. Our results show that hepatic insulin extraction at the three lactate concentrations added was higher than in the control experiments (lactate 1 mmol/l: 263 +/- 51 vs. 765 +/- 114, P < 0.005; lactate 5 mmol/l: 341 +/- 80 vs. 906 +/- 109; P < 0.005; lactate 15 mmol/l: 438 +/- 21 vs. 981 +/- 66 microIU.g-1.30 min-1, P < 0.005). No significant differences were observed in net glucose balance across the liver during perfusion with lactate. Moreover perfused liver displayed a net lactate production during infusion with saline or lactate added at the lower concentrations (1 and 5 mM), whereas at the highest (15 mM), a net lactate uptake by the liver was observed (P < 0.05). Our results suggest that, in perfused rat liver, lactate may increase hepatic insulin clearance. Thus energy fuels such as lactate and nonesterified fatty acid have opposite effects on hepatic insulin clearance and may therefore contribute to the regulation of posthepatic insulin delivery.

Animals↗
PubMed1991

Role of the circulation in measurement of lactate turnover rate.

Previous studies have shown that venous lactate specific activity during arterial tracer lactate infusion differs from arterial lactate specific activity during systemic venous tracer lactate infusion. We performed paired experiments on chronically catheterized rabbits to compare left ventricular (LV) infusion with femoral venous (FV) infusion of L-[U-14C]lactate. Blood was sampled from both the femoral artery (FA) and right ventricle (RV) during both modes of infusion. The mean lactate specific activity measured for each combination (infusion site, sampling site) was (FV,FA) 4,380 +/- 452, (FV,RV) 4,370 +/- 471, (LV,FA) 4,364 +/- 239, and (LV,RV) 3,325 +/- 240 (SE) dpm/mumol. Lactate turnover calculated from the specific activity in the (LV,RV) mode was significantly higher than from the other three modes (P less than 0.001). Models of lactate turnover are discussed demonstrating that the (FV,FA) and analogous modes of infusion sampling measure the turnover rate of lactate molecules that cycle through the circulation. This estimate of turnover is less than the turnover rate by the whole organism to the extent that some produced lactate is metabolized locally without entering the general circulation. The turnover calculated by the (LV,RV) mode overestimates the turnover of circulating lactate and relates to whole body lactate turnover in a complex manner.

Animals↗
PubMed1992

Muscle accounts for glucose disposal but not blood lactate appearance during exercise after acclimatization to 4,300 m.

We hypothesized that the increased blood glucose disappearance (Rd) observed during exercise and after acclimatization to high altitude (4,300 m) could be attributed to net glucose uptake (G) by the legs and that the increased arterial lactate concentration and rate of appearance (Ra) on arrival at altitude and subsequent decrease with acclimatization were caused by changes in net muscle lactate release (L). To evaluate these hypotheses, seven healthy males [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg], on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-D2]glucose (Brooks et al., J. Appl. Physiol. 70: 919-927, 1991) and [3-13C]lactate (Brooks et al., J. Appl. Physiol. 71:333-341, 1991) and rested for a minimum of 90 min, followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 uptake (65 +/- 2% of both acute altitude and acclimatization peak O2 uptake). Glucose and lactate arteriovenous differences across the legs and arms and leg blood flow were measured. Leg G increased during exercise compared with rest, at altitude compared with sea level, and after acclimatization. Leg G accounted for 27-36% of Rd at rest and essentially all glucose Rd during exercise. A shunting of the blood glucose flux to active muscle during exercise at altitude is indicated. With acute altitude exposure, at 5 min of exercise L was elevated compared with sea level or after acclimatization, but from 15 to 45 min of exercise the pattern and magnitude of L from the legs varied and followed neither the pattern nor the magnitude of responses in arterial lactate concentration or Ra. Leg L accounted for 6-65% of lactate Ra at rest and 17-63% during exercise, but the percent Ra from L was not affected by altitude. Tracer-measured lactate extraction by legs accounted for 10-25% of lactate Rd at rest and 31-83% during exercise. Arms released lactate under all conditions except during exercise with acute exposure to high altitude, when the arms consumed lactate. Both active and inactive muscle beds demonstrated simultaneous lactate extraction and release. We conclude that active skeletal muscle is the predominant site of glucose disposal during exercise and at high altitude but not the sole source of blood lactate during exercise at sea level or high altitude.

Acclimatization↗
PubMed1987

Use of lactate as a base in hemodialysis.

The purpose of our study was to investigate the feasibility of using lactate as a complete or partial substitute for acetate in hemodialysis solutions. Six patients, each serving as his own control, were dialyzed once against a dialysis solution containing 40 mM acetate, once against a dialysis solution containing 40 mM DL-lactate and once against a dialysis solution containing 20 mM each of acetate and DL-lactate. Six additional patients underwent hemodialysis using acetate + lactate for a 3-week period, and the blood acid-base values during this period were compared to those obtained during periods when acetate was used. All dialysis treatments were well tolerated without hypotension or other clinical manifestations. When acetate + lactate was used, only a slight delay in the correction of acidosis during dialysis occurred and the net change in the plasma bicarbonate value appeared to be comparable to that measured with acetate. On the other hand, when lactate was used, the increase in the plasma bicarbonate level during and immediately after dialysis was reduced. With acetate + lactate, intradialytic blood D-lactate levels remained between 1 and 2 mM and returned promptly to near baseline within 1 h after dialysis. During 3 weeks of dialysis using acetate + lactate, predialysis plasma bicarbonate values were similar to those achieved when using acetate, but with acetate + lactate, the intradialytic plasma acetate levels were reduced by 50%. The results suggest that DL-lactate merits further evaluation as a potential base for hemodialysis solutions, and that both the D- and the L-lactate isomers are metabolized in maintenance hemodialysis patients.

Acetates↗
PubMed1990

Myocardial lactate release during ischemia in swine. Relation to regional blood flow.

To determine the relation between regional myocardial blood flow, contractile function, and myocardial lactate release during mild-to-moderate regional myocardial ischemia, nine open-chest swine were instrumented for measurement of regional myocardial blood flow (microsphere method), contractile function (sonomicrometry), and hemodynamics. L-[1-14C]Lactate or L-[U-13C]lactate was infused intravenously using a primed continuous infusion technique to quantify regional myocardial lactate release. D-[U-13C]glucose or D-[6-14C]glucose was simultaneously infused to determine the contribution of exogenous glucose to lactate release. Graded coronary ischemia (two to three levels) was created in the left anterior descending coronary arterial distribution by mechanically constricting the artery in five animals or by decreasing flow through a cannulated left anterior descending artery in four animals. In all nine animals, subendocardial blood flow was 0.99 +/- 0.21 (ml/min)/g during control and 0.34 +/- 0.14 (ml/min)/g during the most severe grade of underperfusion (p less than 0.001) in the left anterior descending coronary arterial distribution. Regional myocardial lactate release was 0.15 +/- 0.09 and 1.19 +/- 0.75 mumols/ml, respectively (p less than 0.003). A highly significant inverse correlation was observed between subendocardial blood flow and myocardial lactate release during the graded reductions in blood flow (r = -0.71, p less than 0.001). Results from sonomicrometry showed a significant reduction in contractile ventricular function in the anterior wall during the graded reductions in blood flow. The regional arterial-venous glucose difference increased significantly with underperfusion in the left anterior descending coronary arterial distribution, from 0.14 +/- 0.15 to 0.56 +/- 0.37 mumols/ml (p less than 0.003). The contribution of exogenous glucose to lactate release also increased significantly; 0.04 +/- 0.03 mumols/ml of the lactate came from exogenous glucose during control compared with 0.64 +/- 0.59 mumols/ml during the most severe underperfusion (p less than 0.02). A significant positive correlation exists between lactate release and lactate from exogenous glucose during graded underperfusion (r = 0.96, p less than 0.001). In summary, these data demonstrate a close inverse relation between regional myocardial lactate release and regional subendocardial blood flow during graded ischemia.

Animals↗
PubMed1987

Lactate metabolism of isolated, perfused fetal, and newborn pig hearts.

The role of lactate as an energy substrate in fetal (0.9 gestation) and newborn (2 day old) hearts was investigated in isolated, perfused hearts. Perfusions were performed with Krebs-Henseleit buffer supplemented with glucose (5 mM) in combination with varying concentrations of lactate. Isolated working heart perfusions, in which the heart ejects the buffer at controlled pressure, were carried out with glucose (5 mM) alone and with glucose (5 mM) and lactate (5 mM) combined. With glucose as sole substrate, lactate was produced by the heart and glucose uptake accounted for approximately two-thirds of oxygen consumption. When both glucose and lactate were provided, lactate accounted for more than 80% of oxygen consumption and profoundly suppressed glucose uptake. Further investigations using retrograde perfusion through the aorta demonstrated that lactate uptake was consistently observed when exogenous lactate concentrations exceeded 1.25 mM. Glucose uptake was suppressed with lactate concentrations as low as 0.5 mM and progressive suppression occurred with increasing lactate concentrations. Fetal and newborn pig hearts utilize lactate as a primary substrate for energy production when lactate concentrations are in the physiological range.

Adenosine Triphosphate↗
PubMed1992

Ketogenesis from lactate in rat liver during the perinatal period.

Lactate, which accumulates in neonatal plasma during the first hours after delivery, is used by neonatal tissues as a source of energy and carbon skeleton. In this work, lactate use by rat liver during late gestation (last 3 d) and early neonatal life (6 h postpartum) has been studied. The rate of lactate use by liver was compared with that found with oleate, inasmuch as fatty acids are the main substrates for the liver after the onset of lactation. The main fate of lactate in the liver during the perinatal period was ketone bodies, preferentially over CO2 and lipids. The rate of oxidation of lactate and its incorporation into lipids decreased during late gestation, but the rate of ketogenesis from lactate remained high during this period. After birth, the rate of lactate oxidation sharply increased, but lipogenesis decreased and ketogenesis was maintained. The rates of oleate oxidation and ketogenesis from oleate were two orders of magnitude lower than those from lactate. However, the rate of oleate incorporation into lipids was only 4-fold lower than that observed from lactate under the same circumstances. Our results suggest that lactate is a major substrate for the liver during the perinatal period because it is mainly incorporated into ketone bodies. This may target lactate carbons to different neonatal tissues.

Animals↗
PubMed2006

Activation of the hypothalamo-pituitary-adrenal axis by isolation and restraint stress during lactation in ewes: effect of the presence of the lamb and suckling.

We investigated the effect of the presence and absence of lambs and suckling by lambs to attenuate activation of the hypothalamo-pituitary-adrenal (HPA) axis to isolation and restraint stress in lactating sheep. In experiment 1, blood samples were collected every 10 min from nonlactating (n = 5) and lactating (n = 5) ewes for 4 h before and during stress. In experiment 2, ewes (n = 6) were allocated to 1) nonlactating, 2) lactating with lambs absent, 3) lactating with lambs present but unable to suckle, and 4) lactating with lambs present and able to suckle. Blood samples were collected over 8 h with no stress (control day) and for 4 h before and 4 h during stress (stress day). In experiment 1, the mean (+/-SEM) cortisol concentrations increased significantly (P < 0.05) in nonlactating ewes during stress but did not change in lactating ewes. In experiment 2, cortisol did not vary on the control day or pretreatment of the stress day but increased (P < 0.05) during stress in all groups except lactating ewes with lambs present and able to suckle. The greatest cortisol response occurred in nonlactating ewes followed by lactating ewes with lambs absent and lactating ewes with lambs present but unable to suckle. During stress, the ACTH concentrations increased (P < 0.05) in nonlactating ewes and lactating ewes with lambs absent but not in lactating ewes with lambs present. We conclude that the activity of the HPA axis during isolation and restraint is reduced in lactating ewes and that the presence of lambs increases this level of attenuation.

Adrenocorticotropic Hormone↗
PubMed1996

Transvisceral lactate fluxes during early endotoxemia.

The pathogenesis of hyperlacticemia during sepsis is poorly understood. We investigated the role of lung, kidney, gut, liver, and muscle in endogenous lactate uptake and release during early endotoxemia in an intact, pentobarbital-anesthetized dog model (n = 14). Ultrasonic flow probes were placed around the portal vein and hepatic, renal, and femoral arteries. After splenectomy, catheters were inserted into the pulmonary artery, aorta, and hepatic, left renal, and femoral veins. Whole blood lactate and blood gases from all catheters, organ flows, and cardiac output were measured before and 30 to 45 min after a bolus infusion of Eacherichia coli endotoxin (1 mg/kg). After endotoxin infusion, mean arterial blood lactate level increased from 0.92 +/- 0.11 to 1.60 +/- 0.15 mmol/L (p < 0.0001). Lung lactate flux changed from uptake to release of lactate adding a mean of 9.97 +/- 16.23 mmol/h (p < 0.05) to the systemic circulation. Liver and muscle lactate fluxes remained neutral at all times, while kidney and gut took up lactate from the circulation both before and after endotoxin infusion (mean renal uptake, 2.73 +/- 3.85 mmol/L; p < 0.001; mean gut uptake, 2.46 +/- 2.31 mmol/h; p < 0.002). Except for the kidney, where a decrease in blood flow correlated with diminished uptake, there was no correlation between changes in transvisceral lactate fluxes and organ or systemic oxygen delivery during endotoxemia. A positive correlation between lactate uptake and oxygen consumption during endotoxemia was seen for both gut (p < 0.0001) and kidney (p < 0.002). We conclude that, in the dog, the pathogenesis of endotoxin-induced hyperlacticemia is complex. The lung may be responsible for significant lactate release, and other viscera that normally take up lactate are unable to adequately clear this increased lactate.

Animals↗
PubMed1997

Dangerous curves. A perspective on exercise, lactate, and the anaerobic threshold.

A number of general observations can be made from these recent studies. Lactate is a ubiquitous substance that is produced and removed from the body at all times, even at rest, both with and without the availability of oxygen. It is now recognized that lactate accumulates in the blood for several reasons, not just the fact that oxygen supply to the muscle is inadequate. Lactate production and removal is a continuous process; it is a change in the rate of one or the other that determines the blood lactate level. Rather than a specific threshold, there is most likely a period of time during which lactate production begins to exceed the body's capacity to remove it (through buffering or oxidation in other fibers). It may be appropriate to replace the term "anaerobic threshold" to a more functional description, since the muscles are never entirely anaerobic nor is there always a distinct threshold ("oxygen independent glycolysis" among others has been suggested) Lactate plays a major role as a metabolic substrate during exercise, is the preferred fuel for slow-twitch muscle fibers, and is a precursor for liver gluconeogenesis. The point at which lactate begins to accumulate in the blood, causing an increase in ventilation, is important to document clinically. Irrespective of the underlying mechanism or specific model that describes the process, the physiologic changes associated with lactate accumulation have significant import for cardiopulmonary performance. These include metabolic acidosis, impaired muscle contraction, hyperventilation, and altered oxygen kinetics, all of which contribute to an impaired capacity to perform work. Thus, any delay in the accumulation of blood lactate which can be attributed to an intervention (drug, exercise training, surgical, etc) may add important information concerning the efficacy of the intervention. A substantial body of evidence is available demonstrating that lactate accumulation occurs later (shifting to a higher percentage of Vo2max) after a period of endurance training. In athletes, the level of work that can be sustained prior to lactate accumulation, visually determined, is an accurate predictor of endurance performance. Presumably, these concepts have implications related to vocation/disability among patients with cardiovascular and pulmonary disease, but few such applied studies have been performed outside the laboratory. Blood lactate during exercise and its associated ventilatory changes maintain useful and interesting applications in both the clinical exercise laboratory and the sport sciences. However, the mechanism, interpretation, and application of these changes continue to rely more on tradition and convenience than science.

Anaerobic Threshold↗
PubMed1976

Autoregulatory shift from fructolysis to lactate gluconeogenisis in rat hepatocyte suspensions. The problem of metabolic zonation of liver parenchyma.

Hepatocytes were isolated from fed rats with glucose and insulin and freom fasted rats with glucagon in all media in an attempt to obtain cells which might be fixed preferentially in either the glycolytic or gluconeogenic state. When tested enzymatically, both "fed" and fasted" cells catalyzed glucose formation from lactate (gluconeogenesis) and lactate formation from fructose (fructolysis); lactate formation from glucose may have occurred in "fed" cells. Thus it was impossible, at least in the C3 part of the metabolic pathways between triosephosphate and pyruvate, to fix the hepatocytes in either metabolic state. The shift from glycolysis to gluconeogenesis could be investigated for the C3 part in "fasted" cells with fructose as the glycolytic and lactate as the gluconeogenic substrate. Lactate was first formed from fructose and later reutilized to a large extent. This reconsumption was blocked by the gluconeogenesis inhibitor quinolinate, both when tested enzymatically and radiochemically. Thus fructolysis was shifted to lactate gluconeogenesis. This shift at the assumed phosphoenolpyruvate/pyruvate cycle was autoregulatory, i.e. dependent on substrates and independent of circulating horomes. Maximal velocities and half saturating concentrations were determined for fructose and for lactate as substrates. The kinetic data obtained, especially the sigmoidal pattern of fructolysis, could nicely explain phenomenologically the rather sudden slow-down of lactate production and the shift to lactate consumption. The levels of the metabolites ATP, ADP, AMP, fructose bisphosphate and alanine, which control the enzymes of the assumed phosphoenolypyruvate/pyruvate cycle, were determined in the cytosol and in the mitochondria before and after the shift from fructose glycolysis to lactate gluconeogenesis. The changes observed could not explain the shift. Experiments with [14C] fructose plus unlabelled lactate and reciprocally, with unlabelled fructose plus [14C] lactate, clearly reveled that within the C3 part, glycolysis and gluconeogenesis were catalyzed simultaneously. The simultaneity of and the shift between fructolysis and gluconeogenesis by the liver cell suspension can best be explained by assuming two metabolically different types of hepatocytes rather than one type of hepatocyte with metabolically equal or different cell compartment. In vivo, the different types of hepatocytes would form a gluconeogenic and a glycolytic zone within the liver parenchyma. Since, under normal conditions, the size of these metabolic zones should remain unaltered, the shift from net glycolysis to net gluconeogenesis would be dependent primarily on substrate concentrations (autoregulation).

Adenine Nucleotides↗
PubMed1999

Interaction of late pregnancy and lactation in rats.

The effect of pregnancy on lactation was studied during the third week of lactational pregnancy in postpartum pregnant rats with a delay in implantation of only 1 day (1d-LP rats). In an experimental design in which the suckling litter was prevented from consuming solid food, lactational performance was estimated by weighing the ten-pup suckling litters on days 16-21 of lactation or by measuring maternal weight loss after a nursing spell on day 21. In 1d-LP rats, food consumption as well as lactational performance was lower than it was in nonpregnant lactating rats (L rats) and pregnant-lactating rats with a normal long delay of implantation of at least 6 days (LP rats). The time spent by the pups sucking at the nipples was not different among the three groups, but the number of milk ejections was diminished in 1d-LP dams. Restriction of daily food supply during days 16 to 21 of lactation diminished lactational performance more strongly in 1d-LP rats than it did in L rats; 1d-LP rats conserved protein stores and mobilized fewer minerals than did L rats. The weight and composition of the litter in vitro were not affected by the food restriction. In pregnant-lactating rats (LP and 1d-LP rats), the number of early resorptions was increased in comparison with pregnant rats, showing that lactation can affect the earlier stages of pregnancy. It was concluded that late pregnancy does not affect nursing behaviour, but suppresses lactation by restricting maternal food intake and mobilization of maternal stores. Measurements in serum indicate a causative role for oestradiol, but not for leptin.

Animals↗
PubMed1997

Expression of galanin in hypothalamic magnocellular neurones of lactating rats: co-existence with vasopressin and oxytocin.

Lactation is a physiological condition known to upregulate the expression of the hypothalamic neurohormones, oxytocin and vasopressin, in the rat supraoptic and paraventricular nuclei. Other neuropeptides such as galanin are co-localized in the same magnocellular neurones and their expression has been demonstrated to be regulated by different experimental and physiological conditions. In the present study, we investigated the possible changes in galanin expression during lactation, using in situ hybridization and immunohistochemistry separately or in combination. Galanin messenger RNA concentrations decreased on day 3 of lactation in both the supraoptic and paraventricular nuclei and remained low on day 7 of lactation, but no differences were observed between control and 14-day lactating rats. In parallel, immunopositive cell bodies were almost undetectable on day 7 of lactation and immunoreactivity remained weak after 14 days of lactation, whereas galanin immunoreactive profiles in the supraoptic nucleus were more numerous than in the control group. Moreover, the subcellular distribution of immunostaining changed on day 14 of lactation. Galanin immunoreactivity was confined around the nucleus in the control females, but it became weaker and more homogenously distributed throughout the cytoplasm in the lactating rats. Electron microscopy using a pre-embedding technique confirmed that galanin immunoreactivity was no longer restricted to the Golgi complex, but was apparent throughout in the cytoplasm. Multiple labellings showed galanin and galanin messenger RNA to be co-localized with oxytocin messenger RNA in neurones of the dorsomedial part of the supraoptic nucleus during lactation. Some of those doubly labelled cells also expressed vasopressin messenger RNA in the same conditions as revealed by a triple-labelling procedure. As these co-localizations have not been observed in female control rats, lactation provided an example of a physiological condition inducing oxytocin and galanin co-synthesis in a subpopulation of magnocellular neurones. In conclusion, we have demonstrated plasticity of galanin expression during lactation in the hypothalamic magnocellular neurones. This plasticity could be caused by changes in galanin expression or in galanin processing in magnocellular neurones.

Animals↗
PubMed1992

Effect of DCA administration or endurance training on lactate metabolism in mice during and after exercise.

The purpose of this study was to investigate the effect of the activation of tissue oxidative capacity by dichloroacetate (DCA) administration or endurance training on oxidative removal of lactate, which is the major pathway of lactate metabolism, in mice during prolonged exercise and after supramaximal exercise. DCA administration significantly decreased the blood lactate concentration and activated the oxidative removal of lactate during prolonged exercise. DCA administration did not change lactate metabolism in mice after supramaximal exercise. Endurance training significantly decreased the blood lactate concentration during prolonged exercise and also activated the oxidative removal of lactate. Endurance training significantly increased the recovery of the blood lactate concentration after supramaximal exercise, while it did not activate the oxidative removal of lactate. These results suggest that the activation of the tissue oxidative capacity decreases the blood lactate concentration and also can activate the oxidative removal of lactate during prolonged exercise, while it does not activate the oxidative removal of lactate after supramaximal exercise.

Animals↗
PubMed1993

Effects of an Aspergillus oryzae fermentation extract and other factors on lactate utilization by the ruminal bacterium Megasphaera elsdenii.

The objective of this study was to determine the effects of an Aspergillus oryzae fermentation extract (Amaferm) as well as other factors on lactate utilization by the ruminal bacterium Megasphaera elsdenii B159. Addition of Amaferm or a filter-sterilized Amaferm filtrate stimulated L-lactate uptake by both M. elsdenii and the ruminal selenomonad strain H18. Growth of M. elsdenii in medium that contained DL-lactate (2 g/L), Trypticase, and yeast extract was only slightly stimulated by the addition of 5% (vol/vol) Amaferm filtrate after 24 h. However, growth of M. elsdenii in a similar medium lacking Trypticase and yeast extract was increased over twofold by the addition of either 2 or 5% (vol/vol) Amaferm filtrate. These results suggest that Amaferm provides growth factors (i.e., amino acids, B vitamins) to support growth of M. elsdenii on lactate. There was no inhibition of L-lactate uptake when lactate-grown cells of M. elsdenii were incubated with excess (10 mM) glucose, sucrose, or maltose. In addition, when cells were grown on glucose, sucrose, or maltose rather than lactate there was little difference in L-lactate uptake, suggesting that L-lactate transport in M. elsdenii is not subject to catabolite repression by these soluble sugars. Both K+ and Na+ had little effect on L-lactate uptake. Uptake was unaffected at extracellular pH values between 6.0 and 8.0, whereas pH values of 5.0 and 4.0 increased uptake. In addition, L-lactate uptake was inhibited between 34 and 61% by protonophores. These results suggest that protons may be involved in the uptake of L-lactate by M. elsdenii B159.

Animal Feed↗
PubMed1994

Faecal DL-lactate concentration in 100 gastrointestinal patients.

The relation between faecal DL-lactate and intestinal inflammation or malabsorption was evaluated in 100 nonselected inpatients at a referral center for gastrointestinal disorders. Twenty-one (21%) had DL-lactate concentrations (range, 8-95 mmol/l) above the 95% limit (6.1 mmol/l) in healthy individuals. Inflammatory bowel disease with active proctitis was associated with increased faecal DL-lactate in 11 of 15 patients (73%) (mean, 32 mmol/l; range, 8-95 mmol/l) and in the 1 patient with pouchitis (8 mmol/l), whereas only 1 of 8 patients (13%) with active inflammatory bowel disease without proctitis had L-lactate elevation (25 mmol/l). Among 26 patients with malabsorption and quiescent or noninflammatory bowel disease, 3 of 17 (18%) with preserved colonic function and 3 of 9 (33%) with jejunostomy had increased faecal lactate. Only 2 of 50 (4%) patients with neither active inflammatory bowel disease nor malabsorption had faecal DL-lactate elevation. In vitro bacterial fermentation of most dietary polysaccharides did not cause accumulation of lactate, corresponding to a lack of correlation between faecal carbohydrate excretion and lactate accumulation. An isolated increase in faecal L-lactate was observed in 6 of 13 patients with inflammatory bowel disease, whereas D-lactate was not increased without a simultaneous increase of the L-lactate isomer. In conclusion, the faecal lactate concentration was frequently increased in patients with inflammatory bowel disease and proctitis, occasionally increased in patients with severe malabsorption, and often normal in patients with quiescent inflammatory bowel disease or localized Crohn's ileitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Mammary cell number, proliferation, and apoptosis during a bovine lactation: relation to milk production and effect of bST.

This investigation evaluated mammary cell loss and replacement during lactation and the impact of administration of bST on these processes. During lactation, a gradual decrease in number of mammary epithelial cells within the mammary glands occurs and largely accounts for the decline in milk production with advancing lactation. This decrease is not appreciably impacted by the loss of viable epithelial cells in milk. Rather, the net decline in cell number (approximately 50% during the entire lactation) results from continual death by apoptosis. Accompanying the decline in mammary cell number by apoptosis is a degree of cell renewal. Approximately 0.3% of mammary cells in lactating, nonpregnant cows were labeled by a 24-h in vivo treatment with the thymidine analog, bromodeoxyuridine. During the entire lactation, the number of new cells amounts to approximately 50% of the number of cells initially present. By the end of lactation, most cells present in the mammary gland were formed after calving. Increasing cell replacement or decreasing apoptosis during lactation may provide a means to increase persistency of lactation. Indeed, administration of bST to Holstein cows during midlactation increased the proportion of mammary epithelial cells expressing the nuclear proliferation antigen, Ki-67, from 0.5 to 1.6%. Bovine somatotropin appears to increase the rate of cell renewal in the lactating mammary gland. Knowledge of molecular regulation of apoptosis and cell proliferation should provide a means to modulate cell turnover in the mammary gland. A change in the ratio of epithelial proliferation to cell death during lactation will affect the persistency of lactation.

Animals↗
PubMed2005

Maximization of lactation milk production without decreasing persistency.

This study treats each daily estimated breeding value (EBV) of the lactation as a separate trait to modify the lactation curve on a daily basis. Six selection strategies for improving lactation milk without decreasing persistency were compared: 1) index I(R1), subject to the restriction of equal genetic gains at days in milk (DIM) 60 and 280, 2) I(R2), subject to the restriction of zero gain at DIM 60, 3) desired gains index I(d), designed to increase lactation milk without altering the lactation curve, 4) index I(u), comprising lactation EBV and persistency without standardization, 5) index I(w), consisting of lactation EBV (EBV(L)) and persistency with standardization, and 6) conventional selection on EBV(L) and used as a basis for comparison. Of the 6 selection strategies compared, I(R2) yielded the greatest persistency, but achieved the smallest response in EBV(L), suggesting that it is impractical to increase persistency by inhibiting change in the peak yield. Index I(u) showed the same response in lactation milk as conventional selection on EBV(L), but resulted in the same decreased persistency. Although both I(R1) and I(d) achieved constant persistency, the former produced a greater lactation response (669 kg EBV) than the latter (560 kg EBV). Thus, I(R1) is a viable strategy for improving EBV(L) while holding persistency constant. None of the 6 selection strategies excelled in both lactation milk and persistency. Index I(w) appears to be a reasonable choice for improving both traits, although responses would depend on the relative economic importance of the 2 traits. Differential responses between I(u) and I(w) emphasize the need to weight the EBV of different traits by the inverse of their standard deviations in index construction when the EBV vary widely in variance. The general formula developed here provides a useful genetic means of modifying the lactation curve by restricting differential genetic gains among different days of the lactation.

Animal Nutritional Physiological Phenomena↗