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PubMed1981

Lactate kinetics and individual anaerobic threshold.

Exercise with stepwise increasing work loads until exhaustion leads to a curvilinear increase of lactate in blood and typical lactate kinetics in the post-exercise period. Lactate kinetics in blood during exercise and recovery results from diffusion along gradients between muscle and blood and simultaneous elimination. Therefore, a general diffusion-elimination model is presented from which maximal rate of elimination (Em), individual anaerobic threshold (IAT), gradient between muscle and blood (deltaC-deltaCEm), muscle volume working above the IAT (Vm), individual membrane constant (Mc), quantity of lactate accounting for lactate gradient (Agrad), and whole body lactate (Anet) can be obtained. For demonstration purpose, this model was applied to a highly trained athlete. In this example, all constants and variables mentioned above as well as an equation reflecting individual lactate kinetics were calculated. Furthermore, the IAT was determined in 61 athletes participating in different events. In general, it can be demonstrated that with increasing aerobic capacity the lactate concentration at the IAT decreases. The lactate concentration at the IAT varies interindividually within broad limits, thus emphasizing the need for individual assessment.

Adolescent↗
PubMed2004

Examination of heat stress and stage of lactation (early versus late) on fecal shedding of E. coli O157:H7 and Salmonella in dairy cattle.

Mature, healthy lactating dairy cattle were sampled on two farms in the southwestern United States to examine the effects of heat stress (Experiment I) and stage of lactation (Experiment II) on the fecal shedding of E. coli O157:H7 and Salmonella. To examine the effects of heat stress, fecal samples were collected from 45 cows at 7:00 AM (coolest part of the day) and 5:00 PM (hottest part of the day) in August 2002 on a 250 cow dairy. The study was replicated one month later (n = 170 total samples). A temperature-heat index (THI) was calculated for each sampling time. In Experiment II, stage of lactation was examined by sampling lactating dairy cattle early [< 60 days in milk (DIM)] and late (> 150 DIM) in the lactation cycle in the summer of 2001. The study was replicated the following summer (60 cows/group/replicate; n = 240 total samples). For Experiment I, THI averaged 75 and 82 for the AM and PM samplings, respectively, indicating the cows were beginning to experience heat stress in the morning and by afternoon were in severe heat stress. The shedding of E. coli O157:H7 tended to be higher (p = 0.09) in the afternoon sampling of the first replicate, however was not different in the second replicate or when both replicates were pooled (p > 0.10). Salmonella shedding was not different (p > 0.10) at any sampling time with nearly 100% of the cows positive. Stage of lactation had no effect on the number of cows shedding E. coli O157:H7 (p > 0.10). Salmonella shedding tended to be higher (p = 0.09) in early lactation cows in the first replicate, while in the second replicate more late lactation cows were shedding Salmonella (p < 0.05); however, there were no differences due to stage of lactation when replicates were pooled (p > 0.10). While further research is needed, results of this research highlight the variability in pathogen shedding in healthy dairy cattle and indicate that environmental factors and/or production demands may influence shedding patterns of E. coli O157:H7 and Salmonella.

Animals↗
PubMed1998

Effects of calcium supplementation and lactation on iron status.

Calcium has been shown to inhibit iron absorption. The consequences of chronic calcium supplementation on iron status are unclear, however. As part of a randomized calcium-supplementation trial in lactating and nonlactating women in the postpartum period, we determined whether long-term calcium supplementation and lactation status affected iron stores as measured by serum ferritin concentrations. Subjects (95 lactating and 92 nonlactating) were enrolled at approximately 6 mo postpartum and then randomly assigned to receive either 500 mg Ca as calcium carbonate or a placebo twice daily with meals for 6 mo. Lactating women weaned their infants approximately 2 mo after enrollment (ie, approximately 8 mo postpartum). Calcium supplementation had no effect on serum ferritin concentrations. At the end of the study, geometric mean serum ferritin concentrations were 28.4 microg/L in the calcium-supplemented group and 27.5 microg/L in the placebo group (P > 0.5). Lactation status was significantly related to serum ferritin concentrations. At baseline, serum ferritin concentrations were higher in lactating women than in nonlactating women (47.7 compared with 31.5 microg/L, P < 0.001). In lactating women, serum ferritin concentrations decreased by a mean of 17 microg/L after weaning. By 12 mo postpartum, mean serum ferritin concentrations in women who were previously lactating were not significantly higher than those of nonlactating women (30.5 compared with 25.5 microg/L). These findings provide reassurance that long-term calcium supplementation does not impair iron stores. Furthermore, lactation status should be considered when assessing iron nutriture of women and determinants of iron status in populations.

Adult↗
PubMed2006

Comparison of lactated Ringer's, gelatine and blood resuscitation on intestinal oxygen supply and mucosal tissue oxygen tension in haemorrhagic shock.

OBJECTIVES: To evaluate the effects on intestinal oxygen supply, and mucosal tissue oxygen tension during haemorrhage and after fluid resuscitation with either blood (B; n=7), gelatine (G; n=8), or lactated Ringer's solution (R; n=8) in an autoperfused, innervated jejunal segment in anaesthetized pigs. METHODS: To induce haemorrhagic shock, 50% of calculated blood volume was withdrawn. Systemic haemodynamics, mesenteric venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. A flowmeter was used for measuring mesenteric arterial blood flow. Mucosal tissue oxygen tension (PO(2)muc), jejunal microvascular haemoglobin oxygen saturation (HbO(2)) and microvascular blood flow were measured. Measurements were performed at baseline, after haemorrhage and at four 20 min intervals after fluid resuscitation. After haemorrhage, animals were retransfused with blood, gelatine or lactated Ringer's solution until baseline pulmonary capillary wedge pressure was reached. RESULTS: After resuscitation, no significant differences in macrohaemodynamic parameters were observed between groups. Systemic and intestinal lactate concentration was significantly increased in animals receiving lactated Ringer's solution [5.6 (1.1) vs 3.3 (1.1) mmol litre(-1); 5.6 (1.1) vs 3.3 (1.2) mmol litre(-1)]. Oxygen supply to the intestine was impaired in animals receiving lactated Ringer's solution when compared with animals receiving blood. Blood and gelatine resuscitation resulted in higher HbO(2) than with lactated Ringer's resuscitation after haemorrhagic shock [B, 43.8 (10.4)%; G, 34.6 (9.4)%; R, 28.0 (9.3)%]. PO(2)muc was better preserved with gelatine resuscitation when compared with lactated Ringer's or blood resuscitation [20.0 (8.8) vs 13.8 (7.1) mm Hg, 15.2 (7.2) mm Hg, respectively]. CONCLUSION: Blood or gelatine infusion improves mucosal tissue oxygenation of the porcine jejunum after severe haemorrhage when compared with lactated Ringer's solution.

Animals↗
PubMed1994

Potassium loss during myocardial ischaemia and hypoxia: does lactate efflux play a role?

In heart, the available evidence suggests that transmembrane lactate flux is mediated predominantly by an H(+)-lactate transporter with properties similar, but not identical, to the H(+)-monocarboxylate transporter present in many other tissues. Passive (electro-)diffusion of HL and L- comprise only minor components of total transmembrane lactate flux over the range of lactate concentrations relevant to normal physiological and pathophysiological states. The cardiac H(+)-lactate transporter is non-electrogenic, and transport is partially inhibited by potassium, possibly by competition for the H+ binding site on the carrier. However, K+ is cotransported with lactate very inefficiently, if at all, compared to H+. From these observations, a direct mechanism coupling potassium efflux to lactate efflux, by either an electrogenic or a non-electrogenic mechanism, is unlikely to account for the majority of net potassium loss during myocardial ischaemia or hypoxia, unless the properties of transmembrane lactate flux are markedly altered by the ischaemic and hypoxic environment. Nevertheless, it is intriguing that alterations in pHi, pHo, and transmembrane pH gradients in ischaemic cardiac muscle and fatigued skeletal muscle have effects on net potassium loss that qualitatively parallel the predicted effects on L- efflux. In view of the lack of evidence for a direct link between potassium and lactate efflux in the heart, it is likely that this apparent relationship is either coincidental or indirect, mediated through a series of intermediate transport processes. The nature of these interactions remain to be defined. Further studies are still needed to solve the puzzle of what causes net cellular potassium loss during myocardial ischaemia and hypoxia.

Biological Transport↗
PubMed1976

Gluconeogenesis from lactate in liver of stress-susceptible and stress-resistant pigs.

In vitro rates of lactate conversion to glucose and oxidation to CO2 were determined in livers of stress-susceptible (SS) and stress-resistant (SR) pigs because we hypothesized that livers of SS pigs had a lower capacity than livers of SR pigs to remove lactate from blood. Stress-susceptibility was determined by reaction to halothane at 7 weeks of age. At approximately 9 weeks of age, pigs were assigned to one of three experimental diets. Pigs weighing 95 kg were slaughtered immediately after stress, and liver samples were obtained. Incorporation of lactate into glucose in liver of SS pigs was 38% of that in SR pigs. Addition of either vitamin C or vitamins C and E plus magnesium oxide and collagen extract to a corn-soy diet did not alter lactate conversion to glucose, but depressed lactate oxidation to CO2. No differences were detected in either activities of lactate dehydrogenase, HAD-malate dehydrogenase, phosphoenolpyruvate carboxykinase, fructose-1,6-diphosphatase, and glucose-6-phosphatase or concentration of glycogen in livers of SS and SR pigs. Our data indicate that livers of SS pigs possess a lower capacity to incorporate lactate into glucose and to oxidize lactate to CO2; maximal activities of enzymes measured in this study are not the cause of these differences. Reduced capacity of lactate metabolism in livers of SS pigs seems a part of the etiology of the porcine stress syndrome.

Animals↗
PubMed1980

Glucose and lactate absorption and metabolic interrelationships in lambs switched from low to high concentrate diets.

Two experiments were conducted to measure glucose and lactate absorption and metabolic interrelationships in lambs either switched gradually (experiment 1) or abruptly (experiment 2) from hay to a high concentrate diet. In experiment 1, seven lambs were given primed, continuous, 3-hour infusions of 2-0[3H]glucose, U-[14C]L-lactate and para-aminohippuric acid (portal blood flow indicator) before and after switching from a pelleted hay to a pelleted, 85% concentrate diet. Blood samples were collected at 20-minute intervals during infusions. In experiment 2, four lambs were abruptly switched from a pelleted hay to an all-concentrate diet. Portal and arterial blood samples were collected before and up to 1 week after the diet switch. As a result of increased concentrate intake (experiment 1) net portal absorption and turnover of L-lactate and glucose increased. Percentage of glucose derived from L-lactate decreased. Net portal D-lactate absorption, L-lactate absorption as a percentage of turnover and conversion of L-lactate to glucose were not affected by diet. Lambs in experiment 2 did not become acutely acidotic. The insult to acid-base status peaked 12-16 hours after the diet switch, concurrent with maximum arterio-venous differences in plasma L-lactate and glucose. Arterio venous differences in plasma D-lactate were not significantly affected.

Absorption↗
PubMed1997

Food supplementation during lactation shortens anestrus and elevates gonadotropins in rats.

Breastfeeding delays the resumption of ovulation in women, a phenomenon particularly important in less developed areas. Although human and animal studies indicate that undernutrition extends the period of lactational anestrus, the effect of improving nutritional status during lactation on this time of infecundability, however, is less clear. To assess the effects of food supplementation on duration of lactational anestrus, Sprague-Dawley rats were assigned to one of three dietary groups: 1) control (C), given unrestricted access to diet AIN-76A; 2) food-restricted (FR), fed 50% of the control intake; and 3) food-supplemented (FS), food-restricted until d 0 of lactation and thereafter given unrestricted access to diet AIN-76A. Time to first detectable proestrus was monitored starting on d 10 of lactation. Nursing behaviors and gonadotropin and prolactin concentrations were measured in both intact and ovariectomized dams on d 10, 15 and 20 of lactation; we report these data only on the ovariectomized group, which represents the more appropriate animal model of human reproductive physiology during lactation. Proestrus returned significantly (P < 0.0001) sooner in both FS (18.1 +/- 2.4 d) and C (18.0 +/- 2.9 d) than in FR (28.8 +/- 2.8 d) intact dams. FS rats had higher luteinizing hormone and follicle stimulating hormone concentrations than FR rats (P < 0.0001 for each). Prolactin concentrations were lower on d 20 than on d 10 of lactation for all groups (P < 0.02), but we found no effect of dietary treatment. FS rats spent more time away from their pups (P < 0.05) and experienced less suckling (P < 0.05) than FR rats on d 15 of lactation. These results indicate that food supplementation of previously underfed rats hastens the return of ovulation and is accompanied by alterations in nursing behaviors.

Anestrus↗
PubMed1999

Nutritionally-directed compensatory growth enhances mammary development and lactation potential in rats.

A nutritionally-regulated compensatory growth regimen imposed during a growing period from prepuberty to gestation can significantly affect mammary development and subsequent lactation performance. The objectives of this study were as follows: 1) to determine whether a compensatory nutrition regimen enhances lactation potential for the first and second lactation cycles and 2) to determine the extent to which a compensatory nutrition regimen modulates cell proliferation, differentiation, and apoptosis and expression of genes in mammary tissues of female rats. Female Sprague-Dawley rats (n = 122, 35 d of age) were randomly assigned either to the control group, with free access to diet, or to a stair-step compensatory nutrition feeding regimen, with an alternating 2-2-3-3-wk schedule. The regimen began with an energy-restricted diet (40% restriction) for 2 wk, followed by the control diet for 2 wk; this step was then repeated at 3-wk intervals. Pups of dams from the compensatory nutrition regimen group gained more during mid-lactation than did control group pups. Mammary tissues were obtained from early (d 2) and late (d 19) lactating rats. Mammary tissue from the compensatory nutrition group exhibited increased cell proliferation and greater gamma-glutamyltranspeptidase and ornithine decarboxylase gene expressions than did tissue from the control group during early lactation of both cycles. Mammary tissue from the compensatory nutrition group also had fewer apoptotic cells than tissue from the control group during late lactation of the first lactation cycle. These results suggest that the compensatory nutrition regimen imposed during the peripubertal developmental phase stimulated mammary growth and enhanced lactation performance by affecting the expression of genes that regulate the cell cycle.

Adaptation, Physiological↗
PubMed1999

Lactation in relation to postmenopausal breast cancer.

A modest inverse association between lactation and breast cancer risk has most consistently been observed in premenopausal women, and certain breastfeeding patterns, such as prolonged duration and early age at first lactation, may be important determinants of risk. However, these associations have not generally been observed in relation to postmenopausal breast cancer. As part of a multicenter population-based case-control study, the authors examined postmenopausal breast cancer risk according to breastfeeding characteristics. Breast cancer patients aged 50-79 years were identified from statewide tumor registries in Massachusetts, New Hampshire, and Wisconsin from July 1992 through July 1995. Similarly aged control women were randomly selected from population lists. Information regarding lactation history and breast cancer risk factors was obtained through telephone interviews. This analysis included only data on parous postmenopausal women (3,633 cases and 3,790 controls). After adjustment for age, parity, age at first birth, and other breast cancer risk factors, breastfeeding for at least 2 weeks was associated with a slightly reduced risk of breast cancer in comparison with women who had never lactated (relative risk = 0.87, 95% confidence interval 0.78-0.96). There was only a modest suggestion that increasing cumulative duration of lactation was inversely associated with breast cancer risk; the relative risk for women who had breastfed for > or =24 months was 0.73 (95% confidence interval 0.56-0.94) (p-trend for duration = 0.10). Age at first lactation was not consistently associated with risk. Modest inverse associations appeared to persist even up to 50 years since first lactation. Use of hormones to suppress lactation was not associated with postmenopausal breast cancer, nor was inability to breastfeed related to risk. These results suggest that lactation may have a slight and perhaps long-lasting protective effect on postmenopausal breast cancer risk.

Age Factors↗
PubMed1981

Stimulation of protein synthesis in round spermatids from rat testes by lactate. II. Role of adenosine triphosphate (ATP).

The stimulatory effects of glucose and lactate on protein synthesis by round spermatids (steps 1-8) were further studied. When the cells were incubated with lactate, the response of protein synthesis in round spermatids was closely related to the intracellular level of ATP. The ATP level in spermatids increased to 3.13 +/- 0.20 nmol/10(6) cells from 0.37 +/- 0.02 nmol/10(6) cells after incubation of the cells at 34 degrees C for 60 min in the presence of lactate (20 mM). However, the ATP level fell rapidly to an undetectable level (less than 0.02 nmol/10(6) cells) during incubation for 30 min at 34 degrees C without lactate. The ATP level and the rate of protein synthesis in spermatids increased rapidly when lactate (20 mM) was added to the control cells during incubation. It was also found that incorporation of 32P into ATP was increased by treatment with lactate (20 mM), but glucose (10 mM) had no effect on 32P incorporation into ATP. When the rates of utilization of glucose and lactate by spermatids were examined, using 14C-labeled glucose and lactate, the rate of utilization of lactate was faster than that of glucose. These results suggest that the ATP is probably a major factor in the stimulation of protein synthesis in round spermatids.

Adenosine Triphosphate↗
PubMed1998

Sodium lactate affects sensory and objective characteristics of tray-packed broiler chicken breast meat.

The objective of this study was to determine the antimicrobial properties of sodium lactate solutions adjusted to various pH values. The effectiveness of sodium lactate increases with increased concentrations; however, there are off-flavor development problems associated with increasing concentrations of sodium lactate above 2.0%. This study evaluated the effects of 2% sodium lactate treatments, adjusted to various pH values, on sensory characteristics, instrumental texture, and microbial populations of tray-packed broiler breast meat. Breast meat was treated with either tap water (pH 7.85) or 2% sodium lactate solutions (pH 7.30, 5.50, 5.00, 4.50, and 4.00) and stored at 2 +/- 1 C for 12 d. Approximately 15% of the panelists reported acidic aftertastes in samples treated with pH 5.00 sodium lactate solutions, and 10% of the panelists reported slight sodium or metallic off-flavor in all samples treated with sodium lactate. Instrumental texture measurements were similar (P > 0.05) for all treatments. Sodium lactate (pH 7.30 and 5.50) enhanced (P < 0.05) cooking yields and retarded the growth of spoilage bacteria (pH 5.50 and 5.00). Due to the development of severe discoloration and intense acidic off-odors and -flavors, testing was not conducted on samples treated with pH 4.50 and 4.00 sodium lactate solutions.

Animals↗
PubMed1995

Lactate metabolism in mouse brain astrocytes studied by [13C]NMR spectroscopy.

Astrocytes possess at least two pathways for pyruvate and thus lactate formation involving precursors derived from mitochondria. The present results suggest that malic enzyme is the preferred route for this process. Although overall lactate release appeared to be independent of extracellular lactate concentration, the incorporation of mitochondrial precursors was decreased by starvation, which is known to deplete astrocyte glycogen stores. Using 1-[13C]glucose in the presence of 10 mM lactate led to label incorporation into extracellular lactate which increased from 3.4 +/- 0.4 to 6.5 +/- 0.5% during 4 and 6 h incubation periods, respectively. Lactate production from glycolysis proceeded virtually unaffected by the extracellular lactate concentration. The total amount of lactate in the medium decreased, however, demonstrating that lactate was used as a substrate.

Animals↗
PubMed1980

Lactation suppression.

In spite of a very recent upsurge in breast-feeding in industrialized countries, approximately one-half of parturients are candidates for postpartum lactation suppression. The mechanisms controlling lactation are complex and involve preparation of the breast during pregnancy, stimulation of secretion of milk in the immediate postpartum period, ejection of milk from the alveolar cells, and maintenance of milk production during the period od lactation. The local effects of estrogen and progesterone in the breast prevent milk secretion during pregnancy. With their withdrawal in the postpartum period, the stimulating effect of the anterior pituitary hormone prolactin dominates and milk secretion is initiated and maintained. Milk ejection is accomplished by a neurohormonal reflex resulting in stimulation of the myoepithelial cells of the breast by the posterior pituitary hormone oxytocin. Local stimulation of the breast by suckling is important in initiating the release of oxytocin and also the secretion of prolactin. The suppression of lactation in the postpartum period can be accomplished in approximately 60--70% of females by the use of a tight brassiere and avoidance of stimulation of the nipples. An additional 10% or so of females can be helped with the use of estrogens during the postpartum period. The addition of an androgen to the estrogen increases the success rate of lactation suppression to about 90%. Unfortunately, the use of estrogen alone or in combination with an androgen is accompanied by rebound lactation in a significant number of patients and has been associated with an increased incidence of postpartum thromboembolic disease. Lactation suppression by inhibiting prolactin secretion with synthetic ergot alkaloids such as bromocriptine has been shown to be safe and highly effective both immediately post partum and after lactation has been established. The 2 week period of therapy required with this drug may be unsatisfactory for some patients. If given immediately at delivery, a single injection of testosterone enanthate and estradiol valerate is equally effective in suppressing lactation and, in the young patient who has delivered vaginally, is not associated with significant risk.

Androgens↗
PubMed2003

Lactate is a preferential oxidative energy substrate over glucose for neurons in culture.

The authors investigated concomitant lactate and glucose metabolism in primary neuronal cultures using 13C- and 1H-NMR spectroscopy. Neurons were incubated in a medium containing either [1-13C]glucose and different unlabeled lactate concentrations, or unlabeled glucose and different [3-13C]lactate concentrations. Overall, 13C-NMR spectra of cellular extracts showed that more 13C was incorporated into glutamate when lactate was the enriched substrate. Glutamate 13C-enrichment was also found to be much higher in lactate-labeled than in glucose-labeled conditions. When glucose and lactate concentrations were identical (5.5 mmol/L), relative contributions of glucose and lactate to neuronal oxidative metabolism amounted to 21% and 79%, respectively. Results clearly indicate that when neurons are in the presence of both glucose and lactate, they preferentially use lactate as their main oxidative substrate.

Animals↗
PubMed2000

Metabolic compensation during high energy output in fasting, lactating grey seals (Halichoerus grypus): metabolic ceilings revisited.

Lactation is the most energetically expensive period for female mammals and is associated with some of the highest sustained metabolic rates (SusMR) in vertebrates (reported as total energy throughput). Females typically deal with this energy demand by increasing food intake and the structure of the alimentary tract may act as the central constraint to ceilings on SusMR at about seven times resting or standard metabolic rate (SMR). However, demands of lactation may also be met by using a form of metabolic compensation such as reducing locomotor activities or entering torpor. In some phocid seals, cetaceans and bears, females fast throughout lactation and thus cannot offset the high energetic costs of lactation through increased food intake. We demonstrate that fasting grey seal females sustain, for several weeks, one of the highest total daily energy expenditures (DEE; 7.4 x SMR) reported in mammals, while progressively reducing maintenance metabolic expenditures during lactation through means not explained by reduction in lean body mass or behavioural changes. Simultaneously, the energy-exported in milk is progressively increased, associated with increased lipoprotein lipase activity in the mammary gland, resulting in greater offspring growth. Our results suggest that females use compensatory mechanisms to help meet the extraordinary energetic costs of lactation. Additionally, although the concepts of SusMR and ceilings on total DEE may be somewhat different in fasting lactating species, our data on phocid seals demonstrate that metabolic ceilings on milk energy output, in general, are not constrained by the same kind of peripheral limitations as are other energy-consuming tissues. In phocid seals, the high ceilings on DEE during lactation, coupled with metabolic compensation, are undoubtedly important factors enabling shortened lactation.

Animals↗
PubMed1994

Serum lactogens possessed normal bioactivity in patients with lactation insufficiency.

OBJECTIVE: Insufficient breast milk is the most common reason for premature termination of breast-feeding. The causes of lactation insufficiency are usually multifactorial; in a small percentage of cases it is due to primary lactation failure of unknown origin. The aim of this study was to investigate whether lactation insufficiency of unknown origin could be caused by serum lactogens that had reduced biological activity. DESIGN: Women with lactation insufficiency of unknown origin and normal lactating controls were subjected to a standardized breast-feeding test for assessment of milk production. Thirty minutes later, serum samples were obtained for determination of total lactogen bioactivity, using an in-vitro bioassay, and levels of prolactin (PRL) and growth hormone (GH) using radioimmunoassay (RIA). PATIENTS: Twelve lactating mothers with a clinical diagnosis of lactation insufficiency of unknown origin were compared with 12 matched mothers with normal lactation. MEASUREMENTS: The Nb2 lymphoma cell bioassay was used to measure total lactogen bioactivity in sera. Conventional RIA kits were used to estimate serum PRL and GH concentrations. RESULTS: Mean milk yield on standardized test feed was 21.6 ml for patients and 146.5 ml for controls. In both patient and control groups the total serum lactogen bioactivity ranged from about 150 to 5000 mIU/l, while the serum RIA (PRL+GH) levels ranged from about 350 to over 7000 mIU/l. There was no evidence of lactogens with reduced bioactivity in the patients' sera. CONCLUSION: Lactation insufficiency in the women studied cannot be explained by serum lactogens that possess unusually low bioactivity.

Biological Assay↗
PubMed1995

Effect of lactation on hypothalamic preproenkephalin gene expression.

Enkephalin appears to modulate several aspects of reproductive function in female rats. The purpose of this study was to determine if lactation influences preproenkephalin gene expression in one or more hypothalamic nuclei known to be involved in maternal or reproductive behavior and prolactin secretion. Lactating rats were killed on day 3 (LAC 3) or day 10 (LAC 10) of lactation. Controls consisted of regular 4-day cycling rats that were killed on diestrous day 1, with 9 to 12 females per group. We used in situ hybridization histochemistry to assess preproenkephalin gene expression in individual cells in the medial preoptic nucleus, anterior, medial and posterior arcuate nucleus, magnocellular and parvocellular aspects of paraventricular nucleus, and ventromedial nucleus. Preproenkephalin mRNA in the anterior arcuate nucleus increased to reach significance (P < 0.05) at day 10 of lactation. Levels in the medial arcuate nucleus increased significantly (P < 0.001) by day 3 of lactation (LAC 3) and remained elevated on day 10 (LAC 10). No significant differences between lactating and control rats were detected in preproenkephalin mRNA levels in the posterior arcuate nucleus, medial preoptic nucleus or in the ventromedial nucleus. Substantial levels of preproenkephalin mRNA were found in the paraventricular nucleus, particularly in a limited region of the magnocellular portion. However, these levels did not change with lactation. These data provide evidence for differential regulation of the preproenkephalin gene during lactation. This change may contribute to lactational hyperprolactinemia and suppressed GnRH secretion, leading to reproductive acyclicity.

Animals↗