Glucose metabolism in rat mast cells. Stimulation of the pentose phosphate pathway by compound 48/80

1985 ◽  
Vol 16 (3-4) ◽  
pp. 133-137 ◽  
Author(s):  
Nirmal Chakravarty
Keyword(s):  
Mast Cells ◽  
Glucose Metabolism ◽  
Pentose Phosphate Pathway ◽  
Pentose Phosphate ◽  
Stimulation Of ◽  
Rat Mast Cells

The effect of serum from obese and normal weight men on glucose metabolism in leucocytes

1980 ◽  
Vol 95 (1) ◽  
pp. 134-138 ◽  
Author(s):  
Ole Myking ◽  
Berit Kjøsen ◽  
Hans H. Bassøe
Keyword(s):  
Glucose Metabolism ◽  
Pentose Phosphate Pathway ◽  
Lactate Production ◽  
Normal Weight ◽  
Pentose Phosphate ◽  
Obese Group ◽  
Stimulation Of

Abstract. The influence of pooled serum from either obese or normal weight males on glucose metabolism in human leucocytes has been studied. Leucocytes from normal weight males were incubated with 10–90% pooled serum and either [U-14C], or [1-14C]glucose. Compared to serum from the normal weight males, serum from the obese group had a more stimulating effect on the 14CO2 and [14C]lactate production from [U-14C]glucose and on the 14CO2 production from [1-14C]glucose. The two serum pools had the same stimulating effect on the Embden-Meyerhof pathway as indicated by the formation of [14C]lactate from [1-14C]glucose. Calculations revealed that the activity in the pentose phosphate pathway was stimulated more by serum from obese, than from normal weight males. It is a possibility that increased stimulation of the pentose phosphate pathway may contribute to the development of overweight.

scholarly journals Insulin stimulates glucose metabolism via the pentose phosphate pathway in Drosophila Kc cells

FEBS Letters ◽  
2003 ◽  
Vol 555 (2) ◽  
pp. 307-310 ◽  
Author(s):  
Rolando B. Ceddia ◽  
George J. Bikopoulos ◽  
Arthur J. Hilliker ◽  
Gary Sweeney
Keyword(s):  
Glucose Metabolism ◽  
Pentose Phosphate Pathway ◽  
Pentose Phosphate

scholarly journals Natural polyamines stimulate G-proteins

1992 ◽  
Vol 282 (2) ◽  
pp. 545-550 ◽  
Author(s):  
J L Bueb ◽  
A Da Silva ◽  
M Mousli ◽  
Y Landry
Keyword(s):  
Mast Cells ◽  
Pertussis Toxin ◽  
Inositol Phosphates ◽  
Second Messengers ◽  
G Protein Coupled Receptors ◽  
Extracellular Signals ◽  
Physiological Relevance ◽  
G Protein Coupled ◽  
Stimulation Of ◽  
Rat Mast Cells

The natural polyamines spermine and spermidine, the biosynthetic precursor putrescine and their analogues cadaverine and tyramine stimulate the GTPase activity of purified GTP-binding proteins (Go/Gi) from calf brain reconstituted into phospholipid vesicles. The order of potency was spermine greater than spermidine greater than putrescine = cadaverine greater than tyramine. The physiological relevance of this observation was assessed, showing the same order of potency of polyamines in the stimulation of peritoneal and tracheal rat mast cells. The activation of rat mast cells by polyamines was inhibited by benzalkonium chloride or by a 2 h pretreatment of the cells with pertussis toxin. The increase in inositol phosphates evoked by polyamines was also inhibited by pertussis toxin. Therefore we propose that intracellular polyamines might control the basal level of second messengers and modulate extracellular signals transduced through G-protein-coupled receptors.

The effects of acetate and of pyruvate on the pathways of glucose catabolism in lactating mammary tissue. II. Sheep tissue

1969 ◽  
Vol 36 (3) ◽  
pp. 469-478 ◽  
Author(s):  
R. W. Smith ◽  
R. F. Glascock
Keyword(s):  
Pentose Phosphate Pathway ◽  
Acid Synthesis ◽  
Pentose Phosphate ◽  
Mammary Tissue ◽  
Glucose Catabolism ◽  
Glucose Carbon ◽  
Rat Tissue ◽  
The Relationship ◽  
Stimulation Of

SummaryA study was made of the changes in the rates of oxidation of the C(1), C(2) and C(6) atoms of glucose and in the pathways of glucose catabolism in sheep udder tissue in vitro which occurred when acetate and pyruvate were added.Whereas in rat mammary tissue the rate of oxidation of the C(1) atom of glucose was very much greater than that of the C(6) atom, the ratio of the rates of oxidation of these 2 atoms in sheep tissue was less than 2 when glucose was the only substrate.The addition of acetate resulted in an unequal stimulation of the oxidation of these 2 atoms, with the result that the ratio of their rates of oxidation was about doubled. The rate of oxidation of the C(2) atom was also increased.Acetate also increased the participation of the pentose phosphate pathway in glucose catabolism as measured by the incorporation of the C(1) and C(6) atoms of glucose into fatty acids, lactic acid and glycerol.Pyruvate produced little effect on the rate of oxidation of the C(1) atom but somewhat depressed that of the C(6) atom of glucose. At the same time, it caused a large increase in the participation of the pentose phosphate pathway.These results are discussed with reference to re-cycling of glucose carbon in the pentose phosphate pathway and to the relationship between that pathway and fatty acid synthesis. It is noted that the incorporation of glucose carbon into the 3 intermediates used gave values for the participation of that pathway which were in better agreement than was obtained in rat tissue. It is concluded that triose phosphates are more nearly in equilibrium in sheep than in rat mammary tissue.

scholarly journals The Pentose Phosphate Pathway and Pyruvate Carboxylation after Neonatal Hypoxic-Ischemic Brain Injury

2014 ◽  
Vol 34 (4) ◽  
pp. 724-734 ◽  
Author(s):  
Eva MF Brekke ◽  
Tora S Morken ◽  
Marius Widerøe ◽  
Asta K Håberg ◽  
Ann-Mari Brubakk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glucose Metabolism ◽  
Pentose Phosphate Pathway ◽  
De Novo ◽  
Pentose Phosphate ◽  
Adult Brain ◽  
Resonance Spectroscopy ◽  
Neonatal Brain ◽  
Artery Ligation ◽  
Pyruvate Carboxylation

The neonatal brain is vulnerable to oxidative stress, and the pentose phosphate pathway (PPP) may be of particular importance to limit the injury. Furthermore, in the neonatal brain, neurons depend on de novo synthesis of neurotransmitters via pyruvate carboxylase (PC) in astrocytes to increase neurotransmitter pools. In the adult brain, PPP activity increases in response to various injuries while pyruvate carboxylation is reduced after ischemia. However, little is known about the response of these pathways after neonatal hypoxia-ischemia (HI). To this end, 7-day-old rats were subjected to unilateral carotid artery ligation followed by hypoxia. Animals were injected with [1,2-13C]glucose during the recovery phase and extracts of cerebral hemispheres ipsi- and contralateral to the operation were analyzed using 1H- and 13C-NMR (nuclear magnetic resonance) spectroscopy and high-performance liquid chromatography (HPLC). After HI, glucose levels were increased and there was evidence of mitochondrial hypometabolism in both hemispheres. Moreover, metabolism via PPP was reduced bilaterally. Ipsilateral glucose metabolism via PC was reduced, but PC activity was relatively preserved compared with glucose metabolism via pyruvate dehydrogenase. The observed reduction in PPP activity after HI may contribute to the increased susceptibility of the neonatal brain to oxidative stress.

scholarly journals Wnt5a Increases the Glycolytic Rate and the Activity of the Pentose Phosphate Pathway in Cortical Neurons

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Pedro Cisternas ◽  
Paulina Salazar ◽  
Carmen Silva-Álvarez ◽  
L. Felipe Barros ◽  
Nibaldo C. Inestrosa
Keyword(s):  
Glucose Metabolism ◽  
Wnt Signaling ◽  
Pentose Phosphate Pathway ◽  
Neurodegenerative Disorders ◽  
Metabolic Flux ◽  
High Energy ◽  
Pentose Phosphate ◽  
The Brain ◽  
Glycolytic Rate

In the last few years, several reports have proposed that Wnt signaling is a general metabolic regulator, suggesting a role for this pathway in the control of metabolic flux. Wnt signaling is critical for several neuronal functions, but little is known about the correlation between this pathway and energy metabolism. The brain has a high demand for glucose, which is mainly used for energy production. Neurons use energy for highly specific processes that require a high energy level, such as maintaining the electrical potential and synthesizing neurotransmitters. Moreover, an important metabolic impairment has been described in all neurodegenerative disorders. Despite the key role of glucose metabolism in the brain, little is known about the cellular pathways involved in regulating this process. We report here that Wnt5a induces an increase in glucose uptake and glycolytic rate and an increase in the activity of the pentose phosphate pathway; the effects of Wnt5a require the intracellular generation of nitric oxide. Our data suggest that Wnt signaling stimulates neuronal glucose metabolism, an effect that could be important for the reported neuroprotective role of Wnt signaling in neurodegenerative disorders.

Pathways of glucose catabolism in Mycobacterium smegmatis

1976 ◽  
Vol 22 (9) ◽  
pp. 1374-1380 ◽  
Author(s):  
N. Jayanthi Bai ◽  
M. Ramachandra Pai ◽  
P. Suryanarayana Murthy ◽  
T. A. Venkitasubramanian
Keyword(s):  
Glucose Metabolism ◽  
Carbon Source ◽  
Pentose Phosphate Pathway ◽  
Mycobacterium Smegmatis ◽  
Pentose Phosphate ◽  
Minor Role ◽  
Key Enzymes ◽  
Glucose Catabolism ◽  
A Minor ◽  
Cells Cultured

Glucose metabolism in Mycobacterium smegmatis was investigated by the radiorespirometric method and by assaying for key enzymes of the major energy-yielding pathways. Glucose is oxidized in this organism mainly through the Embden–Meyerhof–Parnas pathway, irrespective of the carbon source used for growth. The pentose phosphate pathway plays only a minor role and its extent depends on the carbon source used for growth. Enzymes of glycolytic and oxidative pathways were detected in cells grown on glucose, glycerol, or pyruvate but enzymes of the Entner–Doudoroff pathway could be detected only in glucose-grown cells. Labeled acetate is utilized by cells cultured on glucose, glycerol, and pyruvate. In all cases more of C1 of acetate was converted to CO2 while incorporation into cellular constituents was maximum from C2 of acetate.

Sign in / Sign up

Export Citation Format

Share Document