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.

scholarly journals The regulation of lipogenesis in vivo in the lactating mammary gland of the rat during the starved-refed transition. Studies wtih acarbose, a glucosidase inhibitor

1987 ◽  
Vol 242 (1) ◽  
pp. 235-243 ◽  
Author(s):  
S W Mercer ◽  
D H Williamson
Keyword(s):  
Mammary Gland ◽  
Time Course ◽  
Chow Diet ◽  
Glucosidase Inhibitor ◽  
Lactating Mammary Gland ◽  
Phosphofructokinase Activity ◽  
Time Course Study ◽  
Fructose 1,6 Bisphosphate

Depression of carbohydrate digestion by oral administration of acarbose, a glucosidase inhibitor, led to a 75% inhibition of the re-activation of lipogenesis in vivo in the mammary gland of 18 h-starved lactating rats refed with 5 g of chow diet. Rates of [1-14C]glucose incorporation in vitro into lipid and CO2 in mammary-gland acini isolated from refed animals were elevated compared with acini from starved rats, but acarbose treatment completely prevented this stimulation. Gastric intubation of glucose led to a large stimulation of lipogenesis in the mammary gland of starved lactating rats, similar to that induced by refeeding with chow diet; this was dependent on the amount of glucose given and the time elapsed between glucose administration and injection of 3H2O for the measurement of lipogenesis. The switch-on of lipogenesis in the mammary gland of starved lactating rats, by refeeding or by intubation of glucose, was associated with a decrease in the ratio of [glucose 6-phosphate]/[fructose 1,6-bisphosphate] in the gland, indicative of an increase in phosphofructokinase activity. A time-course study revealed that the ratio decreased rapidly over the first 30 min of chow refeeding, after which a large surge in lipogenesis was seen. Acarbose, given 25 min after the onset of refeeding, led to a stepwise increase in the ratio, in parallel with the observed decrease in lipogenic activity. It is concluded that the control of lipogenesis in the mammary gland is closely linked to the availability of dietary carbohydrate. An important site of regulation of lipogenesis in the gland appears to be at the level of phosphofructokinase. A possible role of insulin in the regulation of phosphofructokinase activity, and the acute modulation of insulin-sensitivity in the gland during the starved-refed transition, are discussed.

scholarly journals Aerobic lactate production by mammary tissue

1975 ◽  
Vol 146 (1) ◽  
pp. 273-275 ◽  
Author(s):  
A R Elkin ◽  
N J Kuhn
Keyword(s):  
Glucose Uptake ◽  
Lactate Production ◽  
Mammary Glands ◽  
Mammary Tissue ◽  
Metabolic Derangement ◽  
Intact Tissue ◽  
Lactate Formation ◽  
Normal Feature

Glucose uptake and L-lactate production were measured in cell, slice and intact tissue preparations of mammary glands from late-pregnant and lactating rats. The tissues showed extensive conversion of glucose into lactate in vitro, but not in vivo. Therefore aerobic lactate formation is not a normal feature of mammary tissue, but occurs in vitro as the result of some metabolic derangement.

scholarly journals An investigation of arterial insufficiency in the rat hindlimb Correlation of skeletal muscle bloodflow and glucose utilization in vivo

1986 ◽  
Vol 240 (2) ◽  
pp. 395-401 ◽  
Author(s):  
R A Challiss ◽  
D J Hayes ◽  
G K Radda
Keyword(s):  
Skeletal Muscle ◽  
Sciatic Nerve ◽  
Glucose Uptake ◽  
Nerve Stimulation ◽  
Linear Correlation ◽  
Glucose Utilization ◽  
Fold Increase ◽  
Artery Ligation ◽  
Sciatic Nerve Stimulation

Muscle bloodflow and the rate of glucose uptake and phosphorylation were measured in vivo in rats 7 days after unilateral femoral artery ligation and section. Bloodflow was determined by using radiolabelled microspheres. At rest, bloodflow to the gastrocnemius, plantaris and soleus muscles of the ligated limb was similar to their respective mean contralateral control values; however, bilateral sciatic nerve stimulation at 1 Hz caused a less pronounced hyperaemic response in the muscles of the ligated limb, being 59, 63 and 49% of their mean control values in the gastrocnemius, plantaris and soleus muscles respectively. The rate of glucose utilization was determined by using the 2-deoxy[3H]glucose method [Ferré, Leturque, Burnol, Penicaud & Girard (1985) Biochem. J. 228, 103-110]. At rest, the rate of glucose uptake and phosphorylation was statistically significantly increased in the gastrocnemius and soleus muscles of the ligated limb, being 126 and 140% of the mean control values respectively. Bilateral sciatic nerve stimulation at 1 Hz caused a 3-5-fold increase in the rate of glucose utilization by the ligated and contralateral control limbs; furthermore, the rate of glucose utilization was significantly increased in the muscles of the ligated limb, being 140, 129 and 207% of their mean control values respectively. For the range of bloodflow to normally perfused skeletal muscle at rest or during isometric contraction determined in the present study, a linear correlation between the rate of glucose utilization and bloodflow can be demonstrated. Applying similar methods of regression analysis to glucose utilization and bloodflow to muscles of the ligated limb reveals a similar linear correlation. However, the rate of glucose utilization at a given bloodflow is increased in muscles of the ligated limb, indicating an adaptation of skeletal muscle to hypoperfusion.

scholarly journals α-Hederin Inhibits the Growth of Lung Cancer A549 Cells in vitro and in vivo by Increasing SIRT6 Dependent Glycolysis

2020 ◽  
Author(s):  
cong fang ◽  
Yahui Liu ◽  
Lanying Chen ◽  
Yingying Luo ◽  
Yaru Cui ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mouse Model ◽  
Protein Expression ◽  
Glucose Uptake ◽  
A549 Cells ◽  
Lactate Production ◽  
Tumor Xenograft ◽  
Xenograft Mouse Model ◽  
Atp Generation

Abstract Background: α-hederin an effective component of Pulsatilla chinensis (Bunge) Regel, Studies showed that α-hederin exert many pharmacological activities, However, the effect of α-hederin on metabolism is still unclear. This study aimed to illuminate the role of α-hederin in glucose metabolism in lung cancer cells and investigate the molecular mechanism of α-hederin. Methods: CCK8 and colony formation assays were employed to assess the anti-proliferative effects induced by α-hederin. Glucose uptake, ATP generation, and reduced lactate production were measured using kits, and an A549 tumor xenograft mouse model of lung cancer was used to assess the in vivo antitumor effect of α-hederin (5, 10 mg/kg). Glycolytic-related key enzymes hexokinase 2 (HK2), glucose transporters 1 (GLUT1), pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), monocarboxylate transporter (MCT4), c-Myc, Hypoxia inducible factor-1α (HIF-1α) and Sirtuin 6 (SIRT6) protein expression were detected by western blotting and immunohistochemical staining and SIRT6 inhibitors was verified in A549 cells. Results: Our results showed that cell proliferation was significantly inhibited by α-hederin in a dose-dependent manner and that α-hederin inhibited glucose uptake and ATP generation and reduced lactate production. Furthermore, α-hederin remarkably inhibited HK2, GLUT1, PKM2, LDHA, MCT4, c-Myc, HIF-1α and activated SIRT6 protein expression. Using inhibitors, we proved that α-hederin inhibits glycolysis by activating SIRT6. Moreover, a tumor xenograft mouse model of lung cancer further confirmed that α-hederin inhibits lung cancer growth via inhibiting glycolysis in vivo. Conclusions: α-hederin inhibits the growth of non-small cell lung cancer A549 cells by inhibiting glycolysis. The mechanism of glycolysis inhibition includes α-hederin activating the expression of the glycolytic related protein SIRT6.

Mammary gland biopsy does not affect lactation performance in sows

2007 ◽  
Vol 87 (2) ◽  
pp. 281-284 ◽  
Author(s):  
R. N. Kirkwood ◽  
J. Pérez Laspiur ◽  
N. K. Ames ◽  
J. B. Moore ◽  
A. Cegielski ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Feed Intake ◽  
Somatic Cell Count ◽  
Average Daily Gain ◽  
Mammary Tissue ◽  
Molecular Characteristics ◽  
Lactation Performance ◽  
Voluntary Feed Intake ◽  
Daily Gain

To determine morphological and molecular characteristics of porcine mammary tissue in vivo, mammary tissue was collected from 18 sows at 3 to 6 d of lactation and 17 to 19 d of lactation using a biopsy technique. The success of the technique was determined by monitoring lactation performance, as evidenced by sow rectal temperature, voluntary feed intake, milk somatic cell count, and piglet average daily gain. Up to 1.7 g of mammary tissue was collected at each biopsy without decreasing sow feed intake or piglet growth. Key words: Biopsy, mammary gland, lactation, sow

Abstract 344: FNDC5, a PGC1-a-Dependent Myokine, Increases Glucose Utilization and Fatty-Acid Oxidation by AMPK Signaling Pathway

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Ling Tao ◽  
Yi Liu ◽  
Chao Xin ◽  
Weidong Huang ◽  
Lijian Zhang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Glucose Uptake ◽  
Fatty Acid Oxidation ◽  
Glucose Utilization ◽  
C2c12 Cells ◽  
Time Dependent ◽  
Acid Oxidation ◽  
Ampk Signaling

FNDC5 is a hormone secreted by myocytes that could reduce obesity and insulin resistance, However, the exact effect of FNDC5 on glucose and lipid metabolism remain poorly identified; More importantly, the signaling pathways that mediate the metabolic effects of FNDC5 is completely unknown. Here we showed that FNDC5 stimulates β-oxidation and glucose uptake in C2C12 cells in a dose- and time-dependent fashion in vitro (n=8, all P<0.01). In vivo study revealed that FNDC5 also enhanced glucose tolerance in diabetic mice and increased the glucose uptake evidenced by increased [18F] FDG accumulation in hearts by PET scan (n=6, all P<0.05). FNDC5 decreased the expression of gluconeogenesis related molecules (PEPCK and G6Pase) and increased the phosphorylation of ACC, a key modulator of fatty-acid oxidation, both in hepatocytes and C2C12 cells (n=3, all P<0.05). In parallel with its stimulation of β-oxidation and glucose uptake, FNDC5 increased the phosphorylation of AMPK both in hepatocytes and C2C12 cells in a dose- and time-dependent fashion in vitro and in vivo. More importantly, the β-oxidation and glucose uptake, the expression of PEPCK and G6Pase and the phosphorylation of ACC induced by FNDC5 were attenuated by AMPK inhibitor in hepatocytes and C2C12 cells (P<0.05). Most importantly, the FNDC5 induced glucose uptake and phosphorylation of ACC were attenuated in AMPK-DN mice (n=6, all P<0.05). The glucose-lowering effect of FNDC5 in diabetic mice was also attenuated by AMPK inhibitor. Our data presents the direct evidence that FNDC5 stimulates glucose utilization and fatty-acid oxidation by AMPK signaling pathway, suggesting that FNDC5 be a novel pharmacological approach for type 2 diabetes.

scholarly journals Hereditary Nonspherocytic Hemolysis With Erythrocyte Phosphofructokinase Deficiency

Blood ◽  
1972 ◽  
Vol 39 (3) ◽  
pp. 415-425 ◽  
Author(s):  
Larry Waterbury ◽  
Eugene P. Frenkel
Keyword(s):  
Enzyme Activity ◽  
Adenosine Triphosphate ◽  
Lactate Production ◽  
Kinetic Studies ◽  
Glycogen Storage ◽  
Muscle Disease ◽  
Phosphofructokinase Activity ◽  
Phosphofructokinase Deficiency

Abstract Hereditary nonspherocytic hemolysis associated with abnormal erythrocyte phosphofructokinase activity was demonstrated in a young man. Enzyme activity in the propositus, his mother, and maternal grandmother was approximately 60% of normal controls. There was markedly increased lability of enzyme activity on in vitro storage. Kinetic studies revealed increased sensitivity to adenosine triphosphate inhibition. Erythrocyte adenosine triphosphate levels were depressed. The absence of muscle disease and the presence of normal in vivo lactate production following ischemic exercise differentiated this kindred from those with Type VII glycogen storage disease.

scholarly journals Effect of Antibody Binding and Agglutination on Human Platelet Glycolysis: Comparison with Thrombin and Epinephrine

Blood ◽  
1967 ◽  
Vol 30 (5) ◽  
pp. 617-624 ◽  
Author(s):  
SIMON KARPATKIN ◽  
GREGORY W. SISKIND
Keyword(s):  
Glucose Uptake ◽  
Krebs Cycle ◽  
Lactate Production ◽  
Ringer Solution ◽  
Human Platelets ◽  
Solution Ph ◽  
Atp Levels ◽  
Parallel Increase ◽  
Platelet Antibody

Abstract Freshly collected human platelets were washed in a modified human Ringer solution, pH 7.1, and aerobically incubated in the same media for 1 hour in the presence or absence of glucose. The effect of rabbit antihuman platelet antibody or univalent rabbit antihuman platelet antibody fragments (Fab) on platelet glycolysis was determined. Although ATP expenditure and glycogenolytic depletion were noted following platelet agglutination by antibody, these changes were not considered to be of major importance in the in vivo destruction of platelets. Univalent fragments were shown to bind to platelets without causing platelet agglutination or any detectable change in the glycolytic parameters. In contrast, intact platelet antibody resulted in platelet agglutination which was associated with an increase in lactate production and a decrease in ATP levels when platelets were incubated in the absence of glucose. Glucose-6-P levels did not change. When platelets were incubated in the presence of glucose, glucose uptake increased, ATP levels declined and glucose-6-P levels were unchanged. However, the increased glucose uptake was not accompanied by a parallel increase in lactate production as in the case with thrombin or epinephrine-induced agglutination of platelets. It is postulated that platelet antibody activates a glucose-requiring nonglycolytic pathway, perhaps the hexosemonophosphate shunt or the Krebs’ cycle.

scholarly journals Lactate production is the major metabolic fate of glucose in splenocytes and is altered in spontaneously diabetic BB rats

1990 ◽  
Vol 272 (2) ◽  
pp. 445-452 ◽  
Author(s):  
C J Field ◽  
G Wu ◽  
M D Métroz-Dayer ◽  
M Montambault ◽  
E B Marliss
Keyword(s):  
Glucose Utilization ◽  
Lactate Production ◽  
Resting Cells ◽  
Metabolic Fate ◽  
Con A ◽  
Normal Cells ◽  
Immunological Activation ◽  
Proliferation Of Lymphocytes ◽  
Lactate And Pyruvate

Enhanced glucose metabolism is necessary to support the activation and proliferation of lymphocytes. To define further quantitatively the metabolic fates of glucose and assess glucose utilization both in normal cells and in an autoimmune disease with abnormal lymphocytes, [U-14C]glucose conversion into 14CO2 and the production of lactate and pyruvate were measured in splenocytes. Cells from non-diabetes-prone (BBn) and spontaneously diabetic (BBd) rats were studied both freshly isolated ‘resting’ and cultured for 96 h with and without concanavalin A (Con A) stimulation. (1) Lactate was confirmed to be the major end product in both freshly isolated (53% of utilized glucose) and unstimulated cultured (62% of utilized glucose) cells from BBn animals studied at (2-8) x 10(6) cells/ml concentration. The use of concentrations from 10 x 10(6) to 300 x 10(6) cells/ml resulted in progressively less lactate production per 10(6) splenocytes. (2) Cells from BBd animals after stimulation with Con A incorporated less [3H]thymidine and produced significantly less lactate (155 +/- 14 versus 305 +/- 24 nmol/2 h per 10(6) cells) than did BBn cells (P less than 0.05). (3) However, more lactate (101 +/- 8 versus 78 +/- 6 nmol/5 h per 10(6) cells) was produced by ‘resting’ cells from BBd animals compared with BBn (P less than 0.03), and this difference was sustained after 4 days in culture. (4) Significantly greater amounts of pyruvate were produced by BBd than by BBn cells, particularly when stimulated with Con A, suggesting an alteration in the availability of reducing equivalents in BBd cells. (5) These results are consistent with prior metabolic as well as immunological ‘activation’ of cells in vivo in the BB diabetic animals.

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.

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