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.

Neuronal-glial metabolism under depolarizing conditions. A 13C-n.m.r. study.

Abstract: Time courses of incorporation of 13C from 13C-labelled glucose and/or acetate into the individual carbon atoms of amino acids, citrate and lactate in depolarized cerebral tissues were monitored by using 13C-n.m.r. spectroscopy. There was no change in the maximum percentage of 13C enrichments of the amino acids on depolarization, but the maxima were reached more rapidly, indicating that rates of metabolism in both glycolysis and the tricarboxylic acid cycle were accelerated. Although labelling of lactate and of citrate approached the theoretical maximum of 50%, labelling of the amino acids was always below 20%, suggesting that there is a metabolic pool or compartment that is inaccessible to exogenous substrates. Under resting conditions labelling of citrate and of glutamine from [1-13C]glucose was not detected, whereas both were labelled from [2-13C]acetate, which is considered to reflect glial metabolism. In contrast, considerable labelling of these two metabolites from [1-13C]glucose was observed in depolarized tissues, suggesting that the increased metabolism may be due to increased consumption of glucose by glial cells. The labelling patterns on depolarization from [1-13C]glucose alone and from both precursors [( 1-13C]glucose plus [2-13C]acetate) were similar, which also indicates that the changes are due to increased consumption of glucose rather than acetate.

Regulation of hepatic gluconeogenesis and glycogenolysis by catecholamines in rainbow trout during environmental hypoxia

Abstract: This study tests the hypothesis that catecholamines regulate glucose availability during hypoxia in the rainbow trout by activating glycogen phosphorylase (GPase) while inhibiting pyruvate kinase (PK) in the liver. The net result would be an increase in liver glycogenolysis and a reduction of glycolysis and/or enhancement of gluconeogenesis. We used the criteria of Stalmans & Hers (1975) and report much lower resting percent GPase a (active) values (20–30%) than those previously published. Dorsal aortic injections of epinephrine or norepinephrine increased plasma glucose (16–46%), had no effect on liver or muscle glycogen levels, decreased the activity of PK, and increased total and percent GPase a activities. Pre-treatment with the beta-adrenoreceptor antagonist propranolol eliminated these effects. During moderate hypoxia, plasma glucose remained unchanged, while lactate levels increased fourfold. When fish were pre-treated with propranolol, hypoxia depressed plasma glucose levels (−26%), total and percent GPase a, and increased PK activity, suggesting that hypoxia mediated the dephosphorylation of these enzymes. We conclude that catecholamines stimulate hepatic beta-adrenoreceptors during hypoxia and sustain plasma glucose levels by nullifying the deleterious effects of hypoxia on metabolic function. The specific metabolic consequences of these catecholamine-mediated effects are an increase in the activity of the active form of GPase and a reduction in PK activity, which suggests an activation of glycogenolysis and an inhibition of glycolysis and/or activation of gluconeogenesis, respectively.

Elevated glucose levels increase retinal glycolysis and sorbitol pathway metabolism. Implications for diabetic retinopathy.

Abstract: Purpose. To assess effects of elevated glucose levels on retinal glycolysis and sorbitol pathway metabolism. Methods. Freshly isolated retinas from normal male Sprague-Dawley rats were incubated for 2 hours at 37°C, pH 7.45, in Krebs bicarbonate-Hepes buffer containing 5, 10, 20, or 30 mM glucose. Glycolytic metabolites, sorbitol, and fructose were measured in extracts of retina and medium. Results. Elevated glucose levels increased retinal levels of sorbitol and triose phosphates, decreased sn-glycerol-3-phosphate levels, increased lactate and fructose production, and increased the retinal lactate-pyruvate ratio (indicative of an increased cytosolic ratio of free NADH-NAD + like that induced by hypoxia). An inhibitor of aldose reductase (AL 4114) normalized sorbitol, fructose, triose phosphates, and the lactate-pyruvate ratio without affecting lactate production or sn-glycerol 3-phosphate levels. Conclusions. Elevation of retinal glucose levels causes a hypoxia-like redox imbalance pseudo-hypoxia that results from increased oxidation of sorbitol to fructose in the second step of the sorbitol pathway. This redox imbalance provides a plausible explanation for impaired regulation of retinal blood flow (in the absence of vascular structural changes) in humans with diabetes and in nondiabetic acutely hyperglycemic animals. These findings, together with other observations, suggest that this redox imbalance precedes, and may contribute to, hypoxic and ischemic retinopathy associated with diabetes. Invest Ophthalmol Vis Sci. 1995 ;36 :1675-1685.

The oncogene c-Myc coordinates regulation of metabolic networks to enable rapid cell cycle entry.

Abstract: The c-myc proto-oncogene is rapidly activated by serum and regulates genes involved in metabolism and cell cycle progression. This gene is thereby uniquely poised to coordinate both the metabolic and cell cycle regulatory events required for cell cycle entry. However, this function of Myc has not been evaluated. Using a rat fibroblast model of isogenic cell lines, myc(-/-), myc(+/-), myc(+/+) and myc(-/-) cells with an inducible c-myc transgene (mycER), we show that the Myc protein programs cells to utilize both oxidative phosphorylation and glycolysis to drive cell cycle progression. We demonstrate this coordinate regulation of metabolic networks is essential, as specific inhibitors of these pathways block Myc-induced proliferation. Metabolic events temporally correlated with cell cycle entry include increased oxygen consumption, mitochondrial function, pyruvate and lactate production, and ATP generation. Treatment of normal cells with inhibitors of oxidative phosphorylation recapitulates the myc(-/-) phenotype, resulting in impaired cell cycle entry and reduced metabolism. Combined with a kinetic expression profiling analysis of genes linked to mitochondrial function, our study indicates that Myc's ability to coordinately regulate the mitochondrial metabolic network transcriptome is required for rapid cell cycle entry. This function of Myc may underlie the pervasive presence of Myc in many human cancers.