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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.


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Journal ArticleDOI
31 Oct 2014-PLOS ONE
TL;DR: These rapid, sensitive and high-throughput substrate flux analysis methods introduce highly valuable approaches for developing a greater understanding of genetic and epigenetic pathways that regulate cellular metabolism, and the development of therapies that target cancer metabolism.
Abstract: Cancer cells exhibit remarkable alterations in cellular metabolism, particularly in their nutrient substrate preference. We have devised several experimental methods that rapidly analyze the metabolic substrate flux in cancer cells: glycolysis and the oxidation of major fuel substrates glucose, glutamine, and fatty acids. Using the XF Extracellular Flux analyzer, these methods measure, in real-time, the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) of living cells in a microplate as they respond to substrates and metabolic perturbation agents. In proof-of-principle experiments, we analyzed substrate flux and mitochondrial bioenergetics of two human glioblastoma cell lines, SF188s and SF188f, which were derived from the same parental cell line but proliferate at slow and fast rates, respectively. These analyses led to three interesting observations: 1) both cell lines respired effectively with substantial endogenous substrate respiration; 2) SF188f cells underwent a significant shift from glycolytic to oxidative metabolism, along with a high rate of glutamine oxidation relative to SF188s cells; and 3) the mitochondrial proton leak-linked respiration of SF188f cells increased significantly compared to SF188s cells. It is plausible that the proton leak of SF188f cells may play a role in allowing continuous glutamine-fueled anaplerotic TCA cycle flux by partially uncoupling the TCA cycle from oxidative phosphorylation. Taken together, these rapid, sensitive and high-throughput substrate flux analysis methods introduce highly valuable approaches for developing a greater understanding of genetic and epigenetic pathways that regulate cellular metabolism, and the development of therapies that target cancer metabolism.

132 citations

Journal ArticleDOI
TL;DR: A heterogeneous distribution of enzymes of carbohydrate metabolism in the liver lobule seems to be localized preferentially in periportal hepatocytes, whereas the glycolytic enzyme was found to be more active in cells surrounding the pericentral liver cells.
Abstract: Pyruvate kinase and phosphoenolpyruvate carboxykinase activities were determined in microdissected freeze-dried liver cells from the periportal and pericentral area of the liver lobule. Pyruvate kinase activity was measured by a microfluorimetric procedure adapted to 20-200 ng tissue dry weight. In livers from fed rats, its activity was twice as high in the central zone as in the periportal cells; starvation reduced this gradient by decreasing central activities. Phosphoenolpyruvate carboxykinase activity was measured by a microradiochemical technique in 100-300 ng tissue dry weight. In livers from fed rats, this enzyme was nearly 3 times more active in the periportal cells than in the central area. Starvation increased this enzyme in both zones with a more pronounced change in the central cells. The results indicate a heterogeneous distribution of enzymes of carbohydrate metabolism in the liver lobule. Gluconegenesis seems to be localized preferentially in periportal hepatocytes, whereas the glycolytic enzyme was found to be more active in cells surrounding the pericentral liver cells.

132 citations

Journal ArticleDOI
TL;DR: Current findings allow us to understand how lactate production during exercise represents a physiological signal for the activation of a vast transcription network affecting MCT1 protein expression and mitochondrial biogenesis, thereby explaining how training increases the capacity for lactate clearance via oxidation.
Abstract: The intracellular lactate shuttle (ILS) hypothesis holds that lactate produced as the result of glycolysis and glycogenolysis in the cytosol is balanced by oxidative removal in mitochondria of the same cell. Also, the ILS is a necessary component of the previously described cell-cell lactate shuttle (CCLS), because lactate supplied from the interstitium and vasculature can be taken up and used in highly oxidative cells (red skeletal and cardiac myocytes, hepatocytes, and neurons). This ILS emphasizes the role of mitochondrial redox in creating the proton and lactate anion concentration gradients necessary for the oxidative disposal of lactate in the mitochondrial reticulum during exercise and other conditions. The hypothesis was initially supported by direct measurement of lactate oxidation in isolated mitochondria as well as findings of the existence of mitochondrial monocarboxylate transporters (mMCT) and lactate dehydrogenase (mLDH). Subsequently, the presence of a mitochondrial lactate oxidation complex (composed of mMCT1, CD147 (basigin), mLDH, and cytochrome oxidase (COX)) was discovered, which lends support to the presence of the ILS. Most recently, efforts have been made to evaluate the role of lactate as a cell-signaling molecule (i.e., a "lactormone") that is involved in the adaptive response to exercise. Lactate is capable of upregulating MCT1 and COX gene and protein expression. Current findings allow us to understand how lactate production during exercise represents a physiological signal for the activation of a vast transcription network affecting MCT1 protein expression and mitochondrial biogenesis, thereby explaining how training increases the capacity for lactate clearance via oxidation.

132 citations

Journal ArticleDOI
TL;DR: Lactate directly inhibited the phosphorylation of PFK tyrosine residues in skeletal muscle, an important mechanism of the enzyme activation and it is conceivable that lactate exposure can induce inhibition of glucose consumption in tissues.

132 citations

Journal ArticleDOI
TL;DR: Analysis of NAD-dependent respiration and ATP synthesis indicated a strong decrease of Complex I activity in the mitochondria from neoplastic cells, that was confirmed by direct assay of the enzyme redox activity.

132 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20231,429
20221,705
2021581
2020587
2019466
2018391