Glycolysis

About: Glycolysis is a research topic. Over the lifetime, 10593 publications have been published within this topic receiving 507460 citations. The topic is also known as: GO:0006096 & glycolysis.

The acute action of ammonia on rat brain metabolism in vivo

Abstract: 1. Acute NH4+ toxicity was studied by using a new apparatus that removes and freezes the brains of conscious rats within 1s. 2. Brains were removed and frozen 5min after intraperitoneal injection of ammonium acetate (2–3min before the onset of convulsions). Arterial [NH4+] rose from less than 0.01 to 1.74mm at 4–5min. The concentrations of all glycolytic intermediates measured, except glucose 6-phosphate, were increased by the indicated percentage above the control value as follows: glucose (by 41%), fructose 1,6-diphosphate (by 133%), dihydroxyacetone phosphate (by 164%), α-glycerophosphate (by 45%), phosphoenolpyruvate (by 67%) and pyruvate (by 26%). 4. Citrate and α-oxoglutarate concentrations were unchanged and that of malate was increased (by 17%). 5. Adenine nucleotides and Pi concentrations were unchanged but the concentration of creatine phosphate decreased slightly (by 6%). 6. Brain [NH4+] increased from 0.2 to 1.53mm. Net glutamine synthesis occurred at an average rate of 0.33μmol/min per g. 7. The rate of brain glucose utilization was measured in vivo as 0.62μmol/min per g in controls and 0.81μmol/min per g after NH4+ injection. 8. The arteriovenous difference of glucose and O2 increased by 35%. 9. No significant arteriovenous differences of glutamate or glutamine were detected. Thus, although much NH4+ was incorporated into glutamine the latter was not rapidly released from the brain to the circulation. 10. Plasma [K+] increased from 3.3 to 5.4mm. 11. The results indicate that NH4+ stimulates oxidative metabolism but does not interfere with brain energy balance. The increased rate of oxidative metabolism could not be accounted for only on the basis of glutamine synthesis. We suggest that increased extracellular [NH4+] and [K+] decreased the resting transmembrane potential and stimulated Na+,K+-stimulated adenosine triphosphatase activity thus accounting for the increased metabolic rate.

Transformation of human mesenchymal stem cells increases their dependency on oxidative phosphorylation for energy production.

Abstract: An increased dependency on glycolysis for ATP production is considered to be a hallmark of tumor cells. Whether this increase in glycolytic activity is due mainly to inherent metabolic alterations or to the hypoxic microenvironment remains controversial. Here we have transformed human adult mesenchymal stem cells (MSC) using genetic alterations as described for differentiated cells. Our data suggest that MSC require disruption of the same pathways as have been shown for differentiated cells to confer a fully transformed phenotype. Furthermore, we found that MSC are more glycolytic than primary human fibroblasts and, in contrast to differentiated cells, do not depend on increased aerobic glycolysis for ATP production during transformation. These data indicate that aerobic glycolysis (the Warburg effect) is not an intrinsic component of the transformation of adult stem cells, and that oncogenic adaptation to bioenergetic requirements, in some circumstances, may also rely on increases in oxidative phosphorylation. We did find, however, a reversible increase in the transcription of glycolytic enzymes in tumors generated by transformed MSC, indicating this is a secondary phenomenon resulting from adaptation of the tumor to its microenvironment.

Tissue intracellular acid-base status and the fate of lactate after exhaustive exercise in the rainbow trout.

Abstract: Exhaustive ‘burst-type’ exercise in the rainbow trout resulted in a severe acidosis in the white muscle, with pHi dropping from 7.21 to a low of 6.62, as measured by DMO distribution. An accumulation of lactate and pyruvate, depletions of glycogen, ATP and CP stores, and a fluid shift from the extracellular fluid to the intracellular fluid of white muscle were associated with the acidosis. The proton load was in excess of the lactate load by an amount equivalent to the drop in ATP, suggesting that there was an uncoupling of ATP hydrolysis and glycolysis. Initially, lactate was cleared more quickly than protons from the muscle, a difference that was reflected in the blood. It is suggested that during the early period of recovery (0–4 h), the bulk of the lactate was oxidized in situ, restoring pHi to a point compatible with glyconeogenesis. At that time, lactate and H+ were used as substrates for in situ glyconeogenesis, which was complete by 24 h. During this time, lactate and H+ disappearance could account for about 75% of the glycogen resynthesized. The liver and heart showed an accumulation of lactate, and it is postulated that this occurred as a result of uptake from the blood. Associated with the lactate load in these tissues was a metabolic alkalosis. Except for an apparent acidosis immediately after exercise, the acid-base status of the brain was not appreciably affected. Despite the extracellular acidosis, red cell pHi remained nearly constant.

Effects of regional ischemia on metabolism of glucose and fatty acids. Relative rates of aerobic and anaerobic energy production during myocardial infarction and comparison with effects of anoxia.

Abstract: The rate of coronary flow reaching the oxygen-linited heart appears to be crucial in determining the myocardial tissue metabolic response. The tissue metabolic response to anoxia, well studied in hearts perfused with anoxic media, differs in many important ways from the response to ischemia. In regional ischemia (developing infarction) there is still a residual oxygen uptake which is reduced approximately to the same extent as the delivery of O2; there is also decreased delivery of substrates and decreased removal of CO2, H+, and lactate, with increased concentrations of these metabolites. Contents of hexose monophosphates rise rather than fall in anoxia. Measurements of glycolytic intermediates show an initial burst of accelerated glycolytic flux lasting less than 1 minute after coronary artery ligation; thereafter rates of flux decrease to control values or even less at 120 minutes. Relative inhibition of phosphofructokinase (PFK) activity may be explained by a slow rate of fall of ATP and a developing intracellular acidosis. In this model, glucose accounts for a greater part of the residual oxidative metabolism than does free fatty acid (FFA).