Chronic and acute ethanol impair the in vivo glucose uptake by lactating rat mammary gland

1987 ◽  
Vol 7 (10) ◽  
pp. 777-781 ◽  
Author(s):  
S. Vilaró ◽  
O. Viñas ◽  
E. Herrera ◽  
X. Remesar
Keyword(s):  
Mammary Gland ◽  
Glucose Uptake ◽  
Ketone Bodies ◽  
Direct Effects ◽  
Acute Ethanol ◽  
Rat Mammary Gland

Chronic and acute ethanol treatments increased the 3-hydroxybutyrate uptake by lactating rat mammary gland as a consequence of its high afferent concentration, without changing its relative extraction. The uptake of glucose was inhibited in the ethanol treated animals due to intrinsic alterations in the mammary gland metabolism as indicated by the decreased relative extraction and unchanged afferent concentration. These results would suggest that the elevated uptake of ketone bodies in ethanol-treated rats can be responsible, at least in part, for the decrease in glucose uptake by lactating rat mammary gland, although other direct effects of ethanol may be implied.

scholarly journals Regulation of acetyl-CoA carboxylase in rat mammary gland. Effects of starvation and of insulin and prolactin deficiency on the fraction of the enzyme in the active form in vivo

1982 ◽  
Vol 204 (1) ◽  
pp. 273-280 ◽  
Author(s):  
Elizabeth M. McNeillie ◽  
Victor A. Zammit
Keyword(s):  
Mammary Gland ◽  
Enzyme Activities ◽  
Enzyme Concentration ◽  
Acetyl Coa Carboxylase ◽  
Initial Activity ◽  
Acetyl Coa ◽  
Activity Ratios ◽  
Rat Mammary Gland ◽  
Rate Limiting

The ‘initial’ (I), endogenous phosphatase-activated (A) and citrate-activated (C) activities of acetyl-CoA carboxylase were measured in mammary-gland extracts of pregnant and lactating rats. There was a 10-fold increase in the A and C enzyme activities in the transition from early to peak lactation [cf. data of Mackall & Lane (1977) Biochem. J.162, 635–642], but there was no significant increase in the ratio of the initial activity to the A and C activities of the enzyme. Starvation (24h) or short-term (3h) streptozotocin-induced diabetes both resulted in a 40% decrease in I/A and I/C activity ratios. In starvation this was accompanied by a decrease in the absolute values of the A and C activities such that the initial activity in mammary glands of starved animals was 45% that in glands from fed animals. Insulin treatment of starved or diabetic animals 60min before killing increased the I activity without affecting the A or C enzyme activities. Removal of the pups for 24h from animals in peak lactation (weaning) resulted in a marked but similar decrease in all three activities such that, although the initial activity was only 10% of that in suckled animals, the I/A and I/C activity ratios remained high and unaltered. Inhibition of prolactin secretion by injection of 2-bromo-α-ergocryptine gave qualitatively similar results to those during weaning. Simultaneous administration of ovine prolactin completely prevented the effects of bromoergocryptine. It is suggested that the initial activity of acetyl-CoA carboxylase in rat mammary gland is regulated by at least two parallel mechanisms: (i) an acute regulation of the proportion of the enzyme in the active state and (ii) a longer-term modulation of enzyme concentration in the gland. Insulin appeared to mediate its acute effects through mechanism (i), whereas prolactin had longer-term effects on enzyme concentration in the gland. A comparison of initial enzyme activities (I) obtained in the present study with rates of lipogenesis measured in vivo [Agius & Williamson (1980) Biochem. J.192, 361–364; Munday & Williamson (1981) Biochem. J.196, 831–837] gave good agreement between the two sets of data for all conditions studied except for 24h-starved and streptozotocin-diabetic animals. It is suggested that acetyl-CoA carboxylase activity is rate-limiting for lipogenesis in the mammary gland in normal, fed, suckled or weaned animals but that in starved and short-term diabetic animals changes in the activity of the enzyme by covalent modification alone may not be sufficient to maintain the enzyme in its rate-limiting role.

scholarly journals Control of glucose metabolism in isolated acini of the lactating mammary gland of the rat. The ability of glycerol to mimic some of the effects of insulin

1977 ◽  
Vol 168 (3) ◽  
pp. 465-474 ◽  
Author(s):  
A M Robinson ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Utilization ◽  
Homogeneous Population ◽  
Furoic Acid ◽  
Lactating Mammary Gland ◽  
Rat Mammary Gland ◽  
Pyruvate Ratio

Inhibition of glucose uptake by acetoacetate and relief of this inhibition by insulin found previously in slices of rat mammary gland [Williamson, McKeown & Ilic (1975) Biochem. J. 150. 145-152] was confirmed in acini, which represent a more homogeneous population of cells. Glycerol (1mM) behaved like insulin (50 minuits/ml) in its ability to relieve the inhibition of glucose (5 mM) utilization caused by acetoacetate (2 mM) in acini. Both glycerol and insulin reversed the increase in [citrate] and the decrease in [glycerol 3-phosphate] and the [lactate]/[pyruvate] ratio in the presence of acetoacetate. Lipogenesis from 3H2O, [3-14C] acetoacetate, [1-14C]- and [6-14C]-glucose was stimulated, whereas 14CO2 formation from [3-14C]acetoacetate was decreased. Neither insulin nor glycerol relieved the acetoacetate inhibition of glucose uptake when lipogenesis was inhibited by 5-(tetradecyloxy)-2-furoic acid. From measurements of [3-14C]acetoacetate incorporation into lipid in the various situations it is suggested that a cytosolic pathway for acetoacetate utilization may exist in rat mammary gland. In the absence of acetoacetate, glycerol inhibited glucose utilization by 60% and increased both [glycerol 3-phosphate] and the [lactate/[pyruvate] ratio. Possible ways in which glycerol may mimic the effects of insulin are discussed.

scholarly journals Direct effects of phenolic compounds on the mammary gland: in vivo and ex vivo evidence

2021 ◽  
pp. 100034
Author(s):  
Oren Hadaya ◽  
Serge Yan Landau ◽  
Hussein Muklada ◽  
Tova Deutch-Traubmann ◽  
Tzach Glasser ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Phenolic Compounds ◽  
Ex Vivo ◽  
Direct Effects

scholarly journals Rapid inhibition of lipogenesis in vivo in lactating rat mammary gland by medium- or long-chain triacylglycerols and partial reversal by insulin

1980 ◽  
Vol 192 (1) ◽  
pp. 361-364 ◽  
Author(s):  
L Agius ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Glucose Utilization ◽  
Insulin Administration ◽  
Hepatic Lipogenesis ◽  
Medium Chain ◽  
Rat Mammary Gland ◽  
Long Chain ◽  
Partial Reversal

An intragastric load of medium- or long-chain triacylglycerols inhibited lipogenesis in lactating rat mammary gland in vivo by 82 or 89% respectively. This inhibition was reversed partially by insulin administration. Long-chain triacylglycerols inhibited hepatic lipogenesis in vivo but medium-chain triacylglycerols increased it 2-fold. Glucose utilization in vitro by mammary gland acini from triacylglycerol-fed rat was normal.

EFFECTS OF VOLUME AND DISTRIBUTION OF MILK ON THE OXYTOCIN-INDUCED CONTRACTION OF THE LACTATING RAT MAMMARY GLAND IN VIVO

1971 ◽  
Vol 51 (3) ◽  
pp. 437-446 ◽  
Author(s):  
D. J. DeNUCCIO ◽  
C. E. GROSVENOR
Keyword(s):  
Mammary Gland ◽  
Static Pressure ◽  
Pressure Response ◽  
Progressive Reduction ◽  
Equilibrium Pressure ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Rat Mammary Gland ◽  
Different Doses

SUMMARY Milk was added intraductally in 0·2 ml increments to previously emptied mammary glands in rats. Direct microscopic observations of the glands showed that each increment of milk did not distribute evenly either within a single lobule or among lobules. Increase of the intramammary pressure either by i.v. injection of oxytocin or by compression of the gland between thumb and forefinger, distributed the milk more evenly within the gland. These observations led to the routine injection of 1·6–3·2 mu. oxytocin in order to distribute each increment of milk evenly throughout the gland. The intramammary pressure response of the gland to different doses of oxytocin was then determined. The rises in intramammary pressure above equilibrium pressure in response to 0·8 and 1·6 mu. oxytocin increased fourfold on average with increasing gland volume over the compliant portion of the static pressure-volume curve. The slopes of the dose oxytocin-intramammary pressure response lines became progressively steeper and shifted to the left as the volume of the mammary gland increased, indicating a progressive reduction in the dose of oxytocin required to elicit a given response. No differences were noted between rats lactating for 9–13 days and those lactating for 20–24 days. In a related study the duct system of the rat gland was found to contain little fluid even after 8 h of non-suckling, though it became filled swiftly after a single i.v. injection of oxytocin. Non-suckling for 16–24 h was required to overcome passively the resistance to entry of milk from the alveoli.

scholarly journals Regulation of lactating-rat mammary-gland lipogenesis by insulin and glucagon in vivo. The role and site of action of insulin in the transition to the starved state

1984 ◽  
Vol 223 (2) ◽  
pp. 345-351 ◽  
Author(s):  
R G Jones ◽  
V Ilic ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Adaptive Mechanism ◽  
Intracellular Metabolite ◽  
Short Term ◽  
Regulatory Enzymes ◽  
Metabolite Concentrations ◽  
Site Of Action ◽  
Lactating Mammary Gland ◽  
Rat Mammary Gland

Starvation for 6h and 24h caused an 80% and 95% decrease in the rate of mammary-gland lipogenesis respectively in conscious lactating rats. 2. Plasma insulin concentrations decreased and circulating ketone-body concentrations increased with the length of starvation. 3. The inhibition of lipogenesis after 24h starvation was accompanied by increased concentrations of glucose, glucose 6-phosphate and citrate in the mammary gland. Qualitatively similar changes were observed after 6h starvation. 4. Infusion of insulin at physiological concentrations caused a 100% increase in the rate of lipogenesis in fed animals and partially reversed the inhibition of lipogenesis caused by starvation. 5. Infusion of insulin tended to reverse the changes seen in intracellular metabolite concentrations. 4. Infusion of glucagon into fed rats caused no change in the rates of lipogenesis in mammary gland, liver or white adipose tissue. 7. It is concluded that (a) insulin acts physiologically to regulate lipogenesis in the mammary gland, (b) hexokinase and phosphofructokinase are important regulatory enzymes in the short-term control of lipogenesis in the mammary gland, which are under the influence of insulin, and (c) the unresponsiveness of mammary-gland lipogenesis in vivo to infusions of glucagon is consistent with an adaptive mechanism which diverts substrate towards the lactating mammary gland and away from other tissues.

scholarly journals Evaluation of the isolated perfused rat hindquarter for the study of muscle metabolism

1971 ◽  
Vol 124 (3) ◽  
pp. 639-651 ◽  
Author(s):  
N. B. Ruderman ◽  
C. R. S. Houghton ◽  
R. Hems
Keyword(s):  
Glucose Uptake ◽  
Nerve Stimulation ◽  
Ketone Bodies ◽  
Synthetic Medium ◽  
Lactate Production ◽  
Muscle Metabolism ◽  
High Rate ◽  
O2 Consumption ◽  
Glycerol Release

1. The metabolic integrity of a new isolated rat hindquarter preparation was studied. The hindquarter was perfused with a semi-synthetic medium containing aged human erythrocytes. More than 95% of the oxidative metabolism of the preparation was due to muscle, the remainder being due to bone, adipose tissue and, where present, skin. 2. Consumption of O2, glucose utilization, glycerol release and lactate production were similar in the presence and in the absence of the skin, indicating that the latter contributed little to the overall metabolism of the preparation. 3. After 40min of perfusion, tissue concentrations of creatine phosphate, ATP and ADP were similar to those found in muscle taken directly from intact animals. The muscle also appeared normal under the electron microscope. 4. The hindquarter did not lose K% to the medium during a 30min perfusion. In the presence of insulin it had a net K% uptake. 5. Insulin caused a sixfold increase in glucose uptake, stimulated O2 consumption by nearly 40% and depressed glycerol release to less than half the control value. 6. Bilateral sciatic-nerve stimulation caused severalfold increases in O2 consumption and lactate production. In the absence of insulin nerve stimulation also enhanced glucose uptake; in the presence of insulin it did not further increase the already high rate of glucose uptake. 7. Rates of lactate production and O2 consumption of the rat hindquarter in vivo and the isolated perfused hindquarter were very similar. 8. Ketone bodies were a major oxidative fuel in vivo of the hindquarter of a rat starved for 2 days. If the acetoacetate and 3-hydroxybutyrate removed by the tissue were completely oxidized, they would have accounted for 77% of the O2 consumption. 9. Acetoacetate accounted for 84% of the ketone bodies removed by the hindquarter in vivo even though its arterial concentration was half that of 3-hydroxybutyrate. 10. Similar rates of acetoacetate and 3-hydroxybutyrate utilization were observed in the perfused hindquarter. 11. Acetoacetate utilization by the perfused hindquarter was not diminished by the addition of either oleate or insulin to the perfusate. 12. Oxidation of glucose to CO2 accounted for less than 4% of the O2 consumed by the perfused hindquarter in both the presence and the absence of insulin. 13. The results indicate that the isolated perfused hindquarter is a useful tool for studying muscle metabolism. They also suggest that ketone bodies, if present in sufficient concentration, are the preferred oxidative fuel of resting muscle.

scholarly journals Rapid inhibition by intragastric triolein of the re-activation of glucose utilization and lipogenesis in the mammary gland during the starved-refed transition in lactating rats. Evidence for a direct effect of oral lipid on mammary tissue

1988 ◽  
Vol 250 (1) ◽  
pp. 269-276 ◽  
Author(s):  
S W Mercer ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Glucose Uptake ◽  
Time Course ◽  
Glucose Utilization ◽  
Lactate Production ◽  
Dietary Lipid ◽  
Mammary Tissue ◽  
Phosphofructokinase Activity ◽  
Fructose 1,6 Bisphosphate

1. Oral administration of triacylglycerol (triolein) to starved/chow-refed lactating rats suppressed the lipogenic switch-on in the mammary gland in vivo. 2. A time-course study revealed that triolein, administered at 30 min after the onset of refeeding, had no influence on lipogenic rate in the mammary gland between 30 and 60 min, but markedly decreased it between 60 and 90 min. Glucose uptake by the mammary gland (arteriovenous difference) increased by 30 min of refeeding, as did lactate production. Between 30 and 90 min glucose uptake remained high in the control animals, but glucose uptake and net C3-unit uptake were decreased in the triolein-loaded animals by 90 min. 3. Triolein increased [glucose 6-phosphate] in the gland and simultaneously decreased [fructose 1,6-bisphosphate], indicative of a decrease in phosphofructokinase activity. This cross-over occurred at 60 min, i.e. immediately before the inhibition of lipogenesis, and by 90 min had reached ‘starved’ values. 4. Triolein had no effect on plasma [insulin] nor on whole-blood [glucose], [lactate] or [3−hydroxybutyrate]; a small increase in [acetoacetate] was observed. 5. Infusion of the lipoprotein lipase inhibitor, Triton WR1339, abolished the suppression of mammary-gland lipogenesis by triolein and the increase in the [glucose 6-phosphate]/[fructose 1,6-bisphosphate] ratio, suggesting a direct influence of dietary lipid on mammary-gland glucose utilization and phosphofructokinase activity.

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