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PubMed1982

Changes in the proportion of acetyl-CoA carboxylase in the active form in rat liver. Effect of starvation, lactation and weaning.

1. The activity of acetyl-CoA carboxylase (EC 6.4.1.2) in extracts of freeze-clamped liver samples from fed or 24 h-starved virgin, pregnant, lactating and weaned rats was measured (i) immediately after preparation of extracts (;I activity'), (ii) after incubation of extracts with partially purified preparations of either rabbit muscle protein phosphatase 1 [Antoniw, Nimmo, Yeaman & Cohen (1977) Biochem. J.162, 423-433] or rabbit liver phosphatase [Brandt, Capulong & Lee (1975) J. Biol. Chem.250, 8038-8044] (;A activity') and (iii) after incubation with 20mm-potassium citrate before or after incubation with phosphatases (;C activity'). 2. Incubation of liver extracts at 30 degrees C without any additions resulted in activation of acetyl-CoA carboxylase that was shown to be due to dephosphorylation of the enzyme by endogenous protein phosphatase activity. This latter activity was not stimulated by Ca(2+) and/or Mg(2+) but was stimulated by 1 mm-Mn(2+). Incubation of extracts with either of the partially purified phosphatases (0.2-0.5 unit) resulted in faster dephosphorylation and activation. The activity achieved after incubation with either of the exogenously added phosphatases was similar. 3. The A and C activities increased during late pregnancy, were lower than in the virgin rat liver during early lactation and increased by 2-fold in liver of mid-lactating rats. Weaning of mid-lactating rats for 24 h resulted in no change in A and C activities but after 48 h weaning they were significantly lower than those in livers from suckled mothers. 4. The I activity followed a similar pattern of changes as the A and C activities during pregnancy and lactation such that, although the I/A and I/C activity ratios tended to be lower during late pregnancy and early lactation, there were no significant changes in I/A and I/C ratios between lactating and virgin animals. However, these ratios were significantly higher in liver from fed 24 h-weaned animals. 5. Starvation (24 h) resulted in a marked decrease in I activity for all animals studied except early-lactating rats. This was due to a combination of a decrease in the concentration of acetyl-CoA carboxylase in liver of starved animals (A and C activities) and a decrease in the fraction of the enzyme in the active form (lower I/C and I/A ratios). The relative importance of the two forms of regulation in mediating the starvation-induced fall in I activity was about equal in livers of virgin, pregnant and lactating animals. However, the decrease in I/A and I/C ratios was of dominating importance in livers of weaned animals. The A/C activity ratios were the same for livers from all animals studied. 6. The maximal activity of fatty acid synthase was also measured in livers and was highly and positively correlated with the A and C activities of acetyl-CoA carboxylase, suggesting that the concentrations of the two enzymes in the liver were controlled coordinately. 7. It is suggested that the lack of correlation between plasma insulin levels and rates of lipogenesis in the transition from the virgin to the lactating state may be explained by different effects of insulin and prolactin on the concentration of acetyl-CoA carboxylase in the liver and on the fraction of the enzyme in the active form.

Acetyl-CoA Carboxylase↗
PubMed1994

Reconstitution of the lactate carrier from rat skeletal-muscle sarcolemma.

The lactate carrier was solubilized from purified rat skeletal-muscle sarcolemma with the detergent decanoyl-N-methyl-glucamide and the solubilized carrier was reconstituted into phospholipid vesicles. Reconstituted proteoliposomes showed a faster time course of L-lactate uptake than did protein-free liposomes. The rate of L-lactate uptake into the proteoliposomes was inhibited by the lactate-transport inhibitors p-chloromercuribenzenesulphonate, diethyl pyrocarbonate, alpha-cyano-4-hydroxycinnamate and quercetin. In contrast, the anion-exchange inhibitor DIDS (4,4'-di-isothiocyanostilbene-2,2'-disulphonate) had almost no effect on the uptake. The extent of L-lactate uptake at equilibrium was not affected by the presence of the transport inhibitors, but was sensitive to osmotic strength. L-Lactate and pyruvate, but not D-lactate, inhibited L-lactate uptake when present at 10-fold excess. The properties of L-lactate transport in reconstituted proteoliposomes were similar to those observed in native sarcolemmal vesicles, i.e. the lactate carrier seems to retain its transport characteristics during the solubilization and reconstitution steps.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1982

Evidence for a lactate transporter in the plasma membrane of the rat hepatocyte.

1. The rate of uptake in 15 s of L- and D-lactate was studied in isolated hepatocyte preparations from starved rats. 2. Observations were also made of the effect of different concentrations of unlabelled L- and D-lactate on L-[14C]- and D-[14C]-lactate uptake. 3. Lactate uptake into hepatocytes appears to occur by two processes, one saturable and at least partially stereospecific, the other non-saturable, at least up to 28 mmol/l, and probably representing simple non-carrier assisted diffusion. 4. The 15 s uptake of lactate is inhibited by alpha-cyano-3-hydroxycinnamate and by rho-chloromercuriphenylsulphonate but not by the general anion transporter inhibitor 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid, ouabain or the structural analogue DL-rho-hydroxyphenyl-lactate. 5. Transporter-mediated lactate entry into liver cells is enhanced by lowered extracellular pH. 6. It is suggested that the contribution of the diffusion component of lactate entry into the cell may be exaggerated by the artifactual nature of the isolated hepatocyte preparation, and that under some circumstances in vivo, lactate transport into hepatocytes could determine the rate of lactate removal from blood.

Animals↗
PubMed1999

The hypothalamic-pituitary-adrenal axis response to endotoxin is attenuated during lactation.

Pregnancy and lactation are times of prolonged physiological changes affecting the neuroendocrine and immunological systems. One well-characterized change is the neuroendocrine hyporesponsiveness to acute stressful stimuli. We have now designed studies to see whether there is an alteration in the response of the hypothalamic-pituitary-adrenal (HPA) axis to an immunological inflammatory challenge and to ascertain whether lactating animals show altered neural and endocrine responses to inflammatory stimuli. Lactating (day 9-12 postpartum) or virgin control Sprague-Dawley female rats were injected with either 200 microg of endotoxin (lipopolysaccharide, LPS ) or sterile saline given i.p. Trunk blood or jugular blood was collected from the animals at 2 h or hourly over 6 h after injection. Both plasma adrenocorticotropic hormone (ACTH) and corticosterone concentrations were significantly higher in saline treated lactating animals compared with the virgin group. LPS significantly elevated circulating levels of plasma ACTH and corticosterone in both virgin and lactating animals compared with saline controls, however, hormone responses to LPS were significantly reduced in lactating animals relative to virgin controls. Corticosterone-binding globulin concentrations were lower in lactating animals compared to virgin animals and LPS decreased concentrations in virgin, but not lactating rats. Analysis of cfos mRNA in the paraventricular nucleus (PVN) of the hypothalamus revealed that 2 h following injection there was a increase in cfos expression only in the virgin animals treated with LPS, compared to all other treatment conditions. Corticotropin-releasing hormone (CRH) mRNA expression was overall greater in virgin animals, but was increased to similar extent in both virgin and lactating animals treated with LPS. Primary arginine vasopressin (AVP) mRNA transcripts were increased 2 h following LPS injection, but a greater increase in expression was seen in virgin animals. These data demonstrate that there is a lower level of free circulating glucocorticoid in response to inflammatory stimuli and suggests that communication between the immune and endocrine systems may be altered during lactation.

Adrenocorticotropic Hormone↗
PubMed2000

Differential regulation of leptin receptor but not orexin in the hypothalamus of the lactating rat.

During lactation, hypothalamic levels of neuropeptide Y (NPY) and agouti related protein (AGRP) mRNA are increased, while pro-opiomelanocortin (POMC) mRNA is decreased. Serum leptin levels are also decreased during lactation. These changes may underlie the large increases of both food and water intake that occur in concert with milk production. However, additional hypothalamic substances, such as the novel peptide, orexin, may be involved. In addition, in the presence of chronically suppressed levels of serum leptin, there may be a change in leptin receptor expression in the hypothalamus. The objectives of the present study were to determine if orexin and leptin receptor mRNA levels were changed during lactation. Rats were studied on dioestrus of the oestrous cycle or on day 10 postpartum (the lactating animals were suckling eight pups). Orexin mRNA levels in the lateral hypothalamus did not differ between dioestrus and lactation. There was a significant increase in leptin receptor mRNA levels in the supraoptic nucleus during lactation compared to dioestrus. Furthermore, leptin receptor protein, as determined by immunocytochemistry, was colocalized in virtually all vasopressin and oxytocin cells in the supraoptic nucleus. Lactating animals exhibited a decrease in leptin receptor mRNA in the ventromedial hypothalamic nucleus whereas no change was apparent in other hypothalamic areas compared to the dioestrus animals. These results demonstrate that changes in orexin do not appear to contribute to the increase in food intake during lactation. It is likely that the increases in NPY and ARGP, coupled with the decrease in POMC, are primarily responsible for sustaining the chronic hyperphagia of lactation. The changes observed in leptin receptor expression in the hypothalamus, along with the suppression of serum leptin levels, also suggest that the leptin signalling system may play a significant role in the regulation of food and water intake during lactation.

Agouti-Related Protein↗
PubMed2002

Changes in the active membrane properties of rat supraoptic neurones during pregnancy and lactation.

To better understand the plasticity of intrinsic membrane properties of supraoptic magnocellular neuroendocrine cells associated with reproductive function, intracellular recordings were performed in oxytocin (OT) and vasopressin (VP) neurones from virgin, late pregnant (E19-22), and lactating (8-12 days of lactation) rats in vitro, using hypothalamic explants. OT neurones from virgin rats displayed a narrower spike width than neurones from pregnant and lactating rats, characterized by faster rise and decay times. Spike width changes in VP neurones were not as prominent as those observed in OT neurones. In OT neurones, the amplitude and the decay of the afterhyperpolarization following spike trains was significantly larger and faster, respectively, in pregnant and lactating rats compared to virgin rats. These properties did not change during pregnancy and lactation in VP neurones. The incidence of the depolarizing afterpotential following spikes significantly increased from approximately 20% in virgin rats to 40-50% during pregnancy and lactation in OT neurones, but was stable (80-90%) across states in VP neurones. Repetitive firing properties (frequency adaptation, the first interspike interval frequency and frequency-current (F-I) relationship) were altered during pregnancy and lactation in OT neurones, but not VP neurones. The increased incidence of depolarizing afterpotentials in OT neurones enhances excitability, while the increased afterhyperpolarization results in suppression of firing rate. Thus, the changes may favour the short bursting activity seen in OT neurones during lactation. These results confirmed reproductive state-dependent changes in intrinsic membrane properties of OT neurones during lactation, and suggest these changes are in place during late pregnancy. This argues that the plasticity in the electrical properties in OT neurones associated with lactation is not instigated by suckling.

Action Potentials↗
PubMed2000

The metabolism of [3-(13)C]lactate in the rat brain is specific of a pyruvate carboxylase-deprived compartment.

Lactate metabolism in the adult rat brain was investigated in relation with the concept of lactate trafficking between astrocytes and neurons. Wistar rats were infused intravenously with a solution containing either [3-(13)C]lactate (534 mM) or both glucose (750 mM) and [3-(13)C]lactate (534 mM). The time courses of both the concentration and (13)C enrichment of blood glucose and lactate were determined. The data indicated the occurrence of [3-(13)C]lactate recycling through liver gluconeogenesis. The yield of glucose labeling was, however, reduced when using the glucose-containing infusate. After a 20-min or 1-h infusion, perchloric acid extracts of the brain tissue were prepared and subsequently analyzed by (13)C- and (1)H-observed/(13)C-edited NMR spectroscopy. The (13)C labeling of amino acids indicated that [3-(13)C]lactate was metabolized in the brain. Based on the alanine C3 enrichment, lactate contribution to brain metabolism amounted to 35% under the most favorable conditions used. By contrast with what happens with [1-(13)C]glucose metabolism, no difference in glutamine C2 and C3 labeling was evidenced, indicating that lactate was metabolized in a compartment deprived of pyruvate carboxylase activity. This result confirms, for the first time from an in vivo study, that lactate is more specifically a neuronal substrate.

Animals↗
PubMed1990

Increased lactate appearance and reduced clearance during hypoxia in dogs.

In order to assess the effects of severe hypoxia on whole body glucose and lactate kinetics, nine experiments were performed on anesthetized, ventilated mongrel dogs. [U-13C]glucose and [1-14C]lactate (n = 5), or [6-14C]glucose and [U-13C]lactate (n = 4) were infused using the primed-continuous infusion method. Cardiac output was measured by thermodilution. After a control period with 21% O2, inspired O2 was reduced for 90 minutes. Three of the experiments resulted in unstable hemodynamics and lactate levels, and are excluded from the mean data. Arterial PO2 fell from a control level of 106.8 +/- 11.9 to 24.2 +/- 3.5 mmHg during the last 45 minutes of hypoxia, and O2 transport fell to 52% of normoxic values. Arterial lactate concentration and the rate of appearance increased by 428% and 182%, respectively, from control to hypoxia. The metabolic clearance rate for lactate fell by 34%. Arterial glucose levels did not change significantly with hypoxia, but the rate of glucose disappearance rose by 70%, and the rate of glucose conversion to lactate increased 3-fold. It is concluded that acute severe hypoxia in anesthetized dogs causes 1) a large increase in arterial lactate levels, but no significant change in glycemia, 2) a large increase in the rate of lactate disappearance and only a small increase in the rate of glucose disappearance and 3) a fall in the metabolic clearance rate of lactate.

Animals↗
PubMed1993

Plasma cyclic AMP and blood lactate responses to incremental cycling in untrained male subjects.

Recently, it has been suggested that epinephrine influences blood lactate and the lactate threshold during incremental exercise through a beta-adrenergic adenylate cyclase dependent mechanism. We sought to characterize the relationship between the changes in the beta-adrenergic adenylate cyclase system and blood lactate during incremental exercise indirectly through the measurement of plasma cAMP. The relationships of plasma cAMP to blood lactate levels and the lactate threshold were examined in nine untrained male subjects. Each subject performed an incremental exercise test to volitional exhaustion on an electronically-braked cycle ergometer. Although plasma cAMP was rising at the lactate threshold, it did not demonstrate the classic threshold response usually seen in blood lactate. Pairwise matched t-tests were used as a post-hoc test to determine if the successive changes in blood lactate and plasma cAMP between 21.4, 38.6, 58.7, 81.2 and 100% of VO2max were significant. Plasma cAMP was rising between 38.6% and 58.7% and between 58.7% and 81.2% of VO2max, but these changes in plasma cAMP did not reach statistical significance (p > 0.0125) with Bonferoni adjustment. The change in plasma cAMP compared to its previous value as well as the change in plasma cAMP above the resting value was not statistically significant until 81.2% of VO2max. A moderate but significant correlation was observed between blood lactate and plasma cAMP levels (r = 0.612) using blood samples obtained at each workstage in all subjects. The mean correlation between blood lactate and plasma cAMP was 0.75 (S.E. = 0.05) and ranged between 0.58 and 0.97 in individual subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1981

Nutrition--fertility interaction in lactating women of low income groups.

1. Duration of lactational amenorrhoea and interpregnancy interval were related to maternal body-weight in an urban low-income group population of 2250 women. 2. Breast-feeding practices were similar in all the women, none of whom had received any nutritional intervention. 3. In the study group the mean duration of lactation, lactational amenorrhoea and interpregnancy interval (months) were 20.7, 11.2 and 24.2 respectively. 4. Mean duration of lactation was significantly shorter in women whose body-weights were over 55 kg. Duration of lactational amenorrhoea increased with increasing duration of lactation (r 0.5164). 5. The duration of lactational amenorrhoea showed a progressive fall with increasing body-weight (r --0.8139) even when duration of lactation was kept constant. 6. The mean duration of post-partum amenorrhoea in women who did not lactate remained unaltered irrespective of body-weight. 7. The findings suggest that maternal nutritional status modifies return of menstruation only in lactating women.

Amenorrhea↗
PubMed1997

[The effect of different high riboflavin supplements during pregnancy and lactation on performance and erythrocyte glutathione reductase activity of rats].

In two experiments with 160 female Sprague-Dawley rats the influence of various dietary riboflavin supplementations during lactation and during pregnancy and lactation were examined on food intake, body mass, reproduction, hematologic profile and the erythrocyte glutathione reductase activity coefficient (EGR-AC). In the first trial rats were fed a semisynthetic, riboflavin-deficient diet, based on casein and corn starch with various riboflavin supplementations during lactation (0, 2, 4, 6, 8, 10, 12, 40, 400, 4000 mg riboflavin/kg diet). In the second experiment the rats received supplements of 1 and 20 mg riboflavin/kg diet, respectively, during pregnancy. After parturition each group was divided into three sub-groups with riboflavin supplementations during lactation of 1, 5 and 20 mg/kg diet, respectively. Both investigations ended at the 14th day of lactation. Food intake was decreased significantly by 25% and 11% in the groups without riboflavin supplementation or 1 mg riboflavin/kg diet. In the same groups body mass was reduced by 11% and 4%, respectively. With regard to the reproduction parameters the riboflavin supply influenced only the litter mass at the 14th day of lactation and only lactational supply was relevant. In both trials the results of the hematologic profile showed no differences. In riboflavin deficiency (0 or 1 mg riboflavin/kg diet, respectively) the EGR-AC was increased significantly to 1.9 and 1.8, respectively. At the supplementation of 4-5 mg riboflavin/kg diet EGR-AC reached a plateau of 1.45, which was not improved by higher supplements. Concerning the whole reproduction cycle (trial II) there was a stronger influence of the actual lactation-supply on EGR-AC, on the other hand a riboflavin deficiency in pregnancy could be compensated only partially by an optimal supply in lactation. Therefore, based on the parameter EGR-AC an optimal riboflavin supply is recommended for each part of the reproduction cycle. By means of EGR-AC also the riboflavin requirement for lactating rats was derived. Feeding a semisynthetic diet (17.4 MJ ME/kg DM, 20.8% crude protein in DM) a supplementation of 5-6 mg riboflavin/kg or a total content of 6-7 mg/kg diet is recommended.

Animals↗
PubMed1996

Intestinal calcium absorption of women during lactation and after weaning.

We investigated whether intestinal calcium absorption and serum 1,25-dihydroxycholecalciferol (calcitriol) concentrations are higher in women during lactation and after weaning to compensate for calcium lost in breast milk. Measurements were obtained at 4.6 mo postpartum in 24 lactating women and 24 nonlactating women, at 9.6 mo postpartum in 24 lactating women (2.6 mo after complete weaning) and 24 nonlactating women. One-half of the women in each group were randomly assigned to receive 1 g supplemental Ca/d as calcium carbonate. Fractional calcium absorption was measured by using stable isotopic tracers 42Ca and 44Ca. Fractional absorption was 0.32+/-0.02 (+/-SEM) in both lactating and nonlactating women, but was higher in lactating women after weaning (0.37+/-0.02) compared with nonlactating postpartum control subjects (0.31+/-0.02). These effects were independent of calcium intake. Changes in serum calcitriol paralleled changes in fractional absorption. There were no differences in calcitriol concentrations between lactating and nonlactating women, but calcitriol was greater in women after weaning compared with postpartum control subjects. Lactating women who had resumed menses had higher fractional absorption and serum calcitriol than did lactating women who had not. Serum calcium and phosphorus concentrations were greater in lactating compared with nonlactating women; there were no differences between groups after weaning. We conclude that lactation stimulates increases in fractional calcium absorption and serum calcitriol, but the responses are only apparent after weaning or the resumption of menses.

Adult↗
PubMed2004

Bone mass is recovered from lactation to postweaning in adolescent mothers with low calcium intakes.

BACKGROUND: Adolescent mothers may be at increased risk of irreversible bone loss during pregnancy and lactation, particularly when calcium intake is low. OBJECTIVE: Longitudinal changes in bone mass from lactation to postweaning were evaluated in 10 adolescent mothers aged 15-18 y who habitually consumed <500 mg Ca/d. DESIGN: Total-body bone mineral content (TBBMC), total-body bone mineral density (TBBMD), and lumbar spine bone mineral density (LSBMD) were measured at lactation (6-24 wk postpartum) and after weaning (12-30 mo postpartum). Serum hormones (intact parathyroid hormone, estradiol, and prolactin), serum calcium, and markers of bone turnover [urinary N-telopeptide cross-linking region of type I collagen (NTx) and plasma activity of bone alkaline phosphatase] were measured at lactation. RESULTS: TBBMC, total calcium content, TBBMD, and LSBMD increased from lactation to postweaning (P < 0.01). TBBMD and LSBMD were, respectively, 3.6% and 9.7% lower than predicted at lactation and 0.3% and 4.8% lower than predicted in the postweaning period. The increase in age-matched TBBMD adequacy was correlated with the time after resumption of menses (r = 0.86, P < 0.01). Calcium accretion from lactation to postweaning correlated negatively with estradiol (r = -0.86) and prolactin (r = -0.69) and positively with intact parathyroid hormone (r = 0.72) and NTx (r = 0.84) measured at lactation (P < 0.05). CONCLUSIONS: It appears that adolescent mothers with habitually low calcium intakes recover from lactation-associated bone loss after weaning. The rate of bone accretion, however, may not be sufficient to attain peak bone mass at maturity. Hormones regulating bone turnover during lactation may influence bone recovery in adolescent mothers.

Adolescent↗
PubMed1978

Lactate as a precursor of fatty acids in bovine adipose tissue.

In vitro experiments were conducted to determine the rates of lactate, acetate, and glucose conversions to glycerol, CO2, and fatty acids by subcutaneous adipose tissue of cattle. To study the pathway for lactate utilization as a carbon source for lipogenesis, the effect of each of four substates (lactate, acetate, pyruvate, and glucose) on the rate of conversion of the other three was determined. The rates of lactate conversion to fatty acids and to glycerol were greater than those for acetate and glucose. Acetate, however, was oxidized to CO2 at greater rates than either lactate or glucose. Acetate was used for fatty acid synthesis at greater rates than pyruvate was less than that from lactate but greater than that from glucose. Acetate additions to the incubation media decreased the synthetic rates from lactate, pyruvate, and glucose. Pyruvate decreased rates of fatty acid synthesis from glucose but slightly (not statistically significant) stimulated synthesis from lactate and acetate. Lactate decreased glucose and pyruvate utilization but had no effect upon that of acetate. Our results clearly demonstrated that lactate can be used for fatty acid synthesis as well as for glycerogenesis by bovine adipose tissue.

Acetates↗
PubMed1980

Effect of energy intake during pregnancy and lactation on body composition in rats.

A paired feeding experiment involving high (H) and low (L) feeding levels during pregnancy and lactation was conducted using bred and open female rats to determine the effects on body composition. Pregnant rats contained a higher percentage of water in the fat-free body (FFB) than that of non-pregnant rats indicating tissue hydration. Composition of the FFB and fat-free dry matter (FFDM) was not altered by feeding level during pregnancy. During lactation, the feeding levels were either continued H-H and L-L or were changed to H-L or L-H within the lactating or open (non-lactating) pairs. Composition of the FFB and of the FFDM was altered by feeding level during lactation. A high energy intake result in a greater proportional loss of ash than of protein during lactation. In contrast, neither the composition of FFB nor FFDM was altered in the non-lactating rats on similar energy intake regimes. The lactating females had a higher percentage of water in FFB than the non-lactating rats. Although there was variation in water content of FFB and in the composition of FFDM, the correlation between percentage of body water and body fat after the adjustment of effects of pregnancy, lactation, energy and their interaction, was high (r = -0.98).

Animals↗
PubMed1998

Regulation of branched-chain amino acid metabolism in the lactating rat.

There is evidence that during lactation, uptake of the essential branched-chain amino acids (BCAA) by mammary glands exceeds their output in milk protein. In this study, we have measured the potential of lactating rats to catabolize BCAA. The activity, relative protein and specific mRNA levels of the first two enzymes in the BCAA catabolic pathway, branched-chain aminotransferase (BCAT) and branched-chain alpha-keto acid dehydrogenase (BCKD), were measured in mammary gland, liver and skeletal muscle obtained from rat dams at peak lactation (12 d), from rat dams 24 h after weaning at peak lactation and from age-matched virgin controls. Western analysis showed that the mitochondrial BCATm isoenzyme was found in mammary gland. Comparison of lactating and control rats revealed that tissue BCATm activity, protein and mRNA were at least 10-fold higher in mammary tissue during lactation. Values were 1.3- to 1. 9-fold higher after 24 h of weaning. In mammary gland of lactating rats, the BCKD complex was fully active. In virgin controls and weaning dams, only about 20% of the complex was in the active state. Hypertrophy of the liver and mammary gland during lactation resulted in a 73% increase in total oxidative capacity in lactating rats. The results are consistent with increased expression of the BCATm gene in the mammary gland during lactation, whereas oxidation appears to be regulated primarily by changes in activity state (phosphorylation state) of BCKD.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed2003

Response of plasma leptin concentration to jugular infusion of glucose or lipid is dependent on the stage of lactation of Holstein cows.

In this study we investigated the hormonal and metabolite responses to isoenergetic jugular infusions of glucose or lipid in early- and late-lactation Holstein cows. Six Holstein cows were used in a replicated Latin square design with jugular infusions of either 1) control (CON; saline), 2) glucose (GLU; 50% dextrose) or 3) lipid (LIP; 20% Intralipid). Treatments did not affect dry matter intake, with the exception of a hypophagic effect of LIP in late lactation. The GLU-induced hyperglycemia and hyperinsulinemia were greater in late-lactation than in early-lactation cows. The GLU treatment did not affect plasma leptin and insulin-like growth factor-1 (IGF-1) concentrations in early-lactation cows, but it increased them in late-lactation cows. The LIP treatment did not affect plasma leptin, insulin and IGF-1 concentrations in early-lactation cows, despite a marked LIP-induced increase in plasma nonesterified fatty acid and beta-hydroxybutyrate concentrations and a reduction in growth hormone (GH) concentration. Compared with the delayed leptin response to GLU, the stimulatory effect of LIP on leptin secretion in late-lactation cows was relatively rapid and occurred in the absence of any significant changes in plasma insulin, IGF-1 or GH. We propose that insulin-mediated glucose metabolism may be involved in the stimulatory effects of glucose on leptin secretion in late-lactation animals but that the stimulatory effects of lipid are independent of insulin or IGF-1. In early-lactation animals a strong inhibitory effect of GH on leptin expression and release, in addition to low adipose reserves and/or energy balance, might override any short-term stimulatory effect of glucose or lipid on leptin secretion.

Animals↗
PubMed1992

Lactate production in adipose tissue: a regulated function with extra-adipose implications.

Estimates of the quantitative contribution of adipose tissue to whole-body glucose metabolism, previously reported as 1-3%, have been revised to be on the order of 10-30%. These revised estimates come, in part, from a recognition that adipose tissue uses glucose to produce lactate and pyruvate, in addition to CO2 and triglycerides. Lactate production by adipose tissue is modulated in vitro by changes in glucose, insulin, and epinephrine concentrations. In vivo, lactate production is regulated acutely by the animal's nutritional state (fed or fasted) and chronically by the degree of obesity. A strong positive correlation exists between rat fat cell size and relative conversion of glucose to lactate (r = 0.89, P less than 0.001). Diabetes is also associated with markedly increased lactate production in adipocytes. Fat cells from obese or diabetic rats (or humans) can metabolize to lactate as much as 50-70% of the glucose taken up. From these recent studies, a picture is emerging in which the adipose organ may provide lactate for hepatic gluconeogenesis during fasting, and also lactate for hepatic glycogen synthesis after food ingestion. Modulation of adipocyte lactate production and contribution of adipose tissue lactate to the body's fuel economy in physiological and pathological states are the focus of this review.

Adipose Tissue↗