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 Control of glucose metabolism in isolated acini of the lactating mamary gland of the rat. Effects of oleate on glucose utilization and lipogenesis

1978 ◽  
Vol 170 (3) ◽  
pp. 609-613 ◽  
Author(s):  
A M Robinson ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Glucose Metabolism ◽  
Glucose Utilization ◽  
Substrate Utilization ◽  
Inhibitory Effects ◽  
Rat Mammary Gland

Oleate (1mM) had only small inhibitory effects on glucose utilization and lipogenesis in acini isolated from rat mammary gland. Esterification of [1-14C]oleate was unaffected by insulin but were decreased by 60% by acetoacetate (2mM). Glycerol (1mM), but not insulin, relieved this inhibition. These experiments provide further support for the role of acetoacetate in regulating substrate utilization by the gland.

Alterations in mammary-gland blood flow and glucose metabolism in the lactating rat induced by short-term starvation and refeeding

1984 ◽  
Vol 4 (5) ◽  
pp. 421-426 ◽  
Author(s):  
Richard G. Jones ◽  
Dermot H. Williamson
Keyword(s):  
Blood Flow ◽  
Mammary Gland ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Limiting Factor ◽  
Short Term ◽  
Fed State ◽  
Substrate Supply ◽  
Lactating Mammary Gland ◽  
Rate Limiting

Six-hour starvation of lactating rats caused a 75% decrease in mammary-gland lipogenesis. The inhibition of lipogenesis was accompanied by a 45% decrease of blood flow to the mammary gland and a 60% decrease in glucose uptake. Within 2 h of refeeding, lipogenesis and glucose uptake by the gland increased to fed values though blood flow to the gland remained at only 63% of that in the fed state. It is concluded that blood flow, and hence substrate supply, is not a rate-limiting factor for lipogenesis by the lactating mammary gland in the rat.

Regulation of glucose transport and GLUT-1 expression by iron chelators in muscle cells in culture

1995 ◽  
Vol 269 (6) ◽  
pp. E1052-E1058 ◽  
Author(s):  
R. Potashnik ◽  
N. Kozlovsky ◽  
S. Ben-Ezra ◽  
A. Rudich ◽  
N. Bashan
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Glucose Utilization ◽  
Fold Increase ◽  
Muscle Cells ◽  
Iron Chelator ◽  
Whole Body ◽  
Iron Chelators ◽  
Glut 1

Possible association between the degree of iron load and glucose metabolism has been postulated by both in vivo and in vitro studies. Because skeletal muscle plays a major role in whole body glucose utilization, we evaluated the effect of iron chelators deferoxamine (DFO) and bipyridyl (Bip) on glucose metabolism and transport in cultured L6 muscle cells. Bip (0.1 mM) or DFO (0.5 mM) added for 24 h to the culture medium increased glucose consumption, lactate production, and [14C]glucose incorporation into glycogen by approximately twofold. 2-Deoxy-glucose uptake by L6 myotubes increased time dependently, reaching a 5-fold and 2.5-fold increase after 12 h for Bip and DFO, respectively. Insulin induced a 2.5-fold increase in glucose uptake in untreated cells, which was additive to the chelator's effect. Iron chelator-induced glucose transport stimulation was inhibited by cycloheximide (2.5 micrograms/ml), indicating dependence on de novo protein synthesis. Increases in GLUT-1 protein and mRNA concentration, without changes in GLUT-4, were found to be responsible for iron chelator effects. We conclude that L6 cells adapt to reduction in iron availability by increasing glucose utilization through an enhanced expression of GLUT-1, without losing their physiological response to insulin.

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 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.

Alterations of glucose metabolism during perfusion of rat lung with paraquat.

1978 ◽  
Vol 234 (6) ◽  
pp. E653 ◽  
Author(s):  
D J Bassett ◽  
A B Fisher
Keyword(s):  
Glucose Metabolism ◽  
Redox State ◽  
Glucose Utilization ◽  
Lactate Production ◽  
Mitochondrial Metabolism ◽  
Co2 Production ◽  
Bicarbonate Buffer ◽  
Enzymatic Reduction ◽  
14Co2 Production ◽  
Pyruvate Ratio

Isolated perfused rat lungs were used to investigate effects of paraquat on lung glucose metabolism. Lungs were ventilated with 5% CO2 in air and perfused with Krebs-Ringer bicarbonate buffer, pH 7.4, containing albumin and 5.5 mM radiolabeled D-glucose. Control lung glucose utilization, estimated from rate of 3H2O production from [5-3H]glucose, was 44 mumol/h-g dry wt. Pentose cycle activity, based on 14CO2 specific yields at the end of perfusions with [1-14C]- and [6-14C]glucose, was 14% of glucose utilization. During perfusion with 1.5 mM paraquat, glucose utilization increased 28%, 14CO2 production via the pentose cycle increased 182% (P less than 0.005), CO2 production via mitochondrial metabolism increased 39% (P less than 0.02), and the rate of lactate production increased 28% (P less than 0.05). Pyruvate production and the lactate-to-pyruvate ratio were not significantly altered. The data indicate that interaction of paraquat with the lung results in increased turnover of cytoplasmic NADPH and increased mitochondrial metabolism, but no significant change in cytoplasmic redox state. The findings are compatible with intracellular enzymatic reduction of paraquat by an NADPH-requiring reductase.

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.

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