Localization of an Infectious Lesion and Glucose Metabolism via the Pentose Phosphate Pathway

Nature ◽  
1964 ◽  
Vol 201 (4921) ◽  
pp. 825-827 ◽  
Author(s):  
PETER BEACONSFIELD ◽  
AMILCARE CARPI
FEBS Letters ◽  
2003 ◽  
Vol 555 (2) ◽  
pp. 307-310 ◽  
Author(s):  
Rolando B. Ceddia ◽  
George J. Bikopoulos ◽  
Arthur J. Hilliker ◽  
Gary Sweeney

2014 ◽  
Vol 34 (4) ◽  
pp. 724-734 ◽  
Author(s):  
Eva MF Brekke ◽  
Tora S Morken ◽  
Marius Widerøe ◽  
Asta K Håberg ◽  
Ann-Mari Brubakk ◽  
...  

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.


2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Pedro Cisternas ◽  
Paulina Salazar ◽  
Carmen Silva-Álvarez ◽  
L. Felipe Barros ◽  
Nibaldo C. Inestrosa

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.


1976 ◽  
Vol 22 (9) ◽  
pp. 1374-1380 ◽  
Author(s):  
N. Jayanthi Bai ◽  
M. Ramachandra Pai ◽  
P. Suryanarayana Murthy ◽  
T. A. Venkitasubramanian

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.


2005 ◽  
Vol 17 (2) ◽  
pp. 293 ◽  
Author(s):  
R. Krisher

Glucose metabolism is an indicator of oocyte developmental competence, and is also correlated with meiotic maturation. In vitro maturation of porcine oocytes with the pentose phosphate pathway (PPP) inhibitor diphenyleneiodonium (DPI) blocks meiotic progression to metaphase II. The objectives of this study were (1) to examine the reversibility of meiotic arrest induced by DPI; and (2) to overcome metabolically induced meiotic arrest by the addition of PPP end products and cofactors downstream of DPI inhibition. Oocytes were matured for 40 h in standard (defined) maturation media containing 0, 25, 50, or 100 nM DPI. At that time half the oocytes in each treatment (TRT) were fixed, and half were moved into standard maturation medium with no DPI for an additional 40 h, at which time all remaining oocytes were fixed. Two oocytes were matured for 40 h in one of 11 media: standard (defined) maturation medium (STND), standard with 50 nM DPI (DPI), standard with 50 nM DPI and 0.25, 2.5, or 5 mM phosphoribose diphosphate (PRPP), nicotinamide adenine dinucleotide phosphate (NADP), or ribose-5-phosphate (R5P). Additionally, 10 mM R5P and 12.5 mM PRPP were examined. All oocytes were fixed. Oocytes were assigned a meiotic score; germinal vesicle (GV) = 1, GV breakdown (GVBD) = 2, condensed chromatin (CC) = 3, metaphase I (MI) = 4, anaphase (A) = 5, telophase (T) = 6, and metaphase II (MII) = 7. Immature oocytes were classified as those at GV or GVBD stages, and mature oocytes as those at A, T or MII stages. Data were analyzed by ANOVA and are presented as mean ± SEM. After 40 h of arrest (n = 79–87/TRT), increasing concentrations of DPI significantly increased the % of immature oocytes (0, 7.2 ± 2.9; 25, 26.4 ± 4.8; 50, 53.2 ± 5.7; 100, 75.9 ± 4.8) and decreased the % of mature oocytes (0, 73.5 ± 4.9; 25, 52.9 ± 5.4; 50, 20.3 ± 4.6; 100, 0). After an additional 40 hours in standard maturation medium (n = 89–93/TRT), there was no difference in the % of immature oocytes between treatments (0, 7.5 ± 2.8; 25, 14.4 ± 3.7; 50, 13.0 ± 3.5; 100, 9.0 ± 3.0) although the % of mature oocytes significantly decreased with increasing DPI concentration (0, 90.3 ± 3.1; 25, 68.9 ± 4.9; 50, 35.9 ± 5.0; 100, 10.1 ± 3.2). Data from experiment 2 are presented below. Meiotic maturation is significantly inhibited by DPI in a dose-dependent manner. Ability of the oocyte to reach MII following 40 h of arrest is also concentration-dependent, although all treatments resulted in GVBD following removal from DPI. Metabolic arrest can be overcome, resulting in numbers of mature oocytes equal to standard controls, by NADP and PRPP but only moderately by R5P. These data demonstrate that glucose metabolism via the PPP is a critical control mechanism of meiotic maturation in porcine oocytes. Table 1. Effect of PPP cofactors and end products on overcoming metabolically induced meiotic arrest in porcine oocytes


1980 ◽  
Vol 95 (1) ◽  
pp. 134-138 ◽  
Author(s):  
Ole Myking ◽  
Berit Kjøsen ◽  
Hans H. Bassøe

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.


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