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Bioenergetics
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
The process by which glucose can be catabolized to produce energy is termed glycolysis. Two sources of glucose are available: blood glucose and glucose derived from the breakdown of stored glycogen. The glycolytic process is catalyzed by a series of nine cytoplasmic enzymes (Figure 2.3). As a result of exercise intensity, glycolysis can proceed at either a faster (anaerobic) or a slower (aerobic) rate. In the past, the terms anaerobic and aerobic glycolysis have been used based on the final fate of pyruvate, either being converted to lactate (anaerobic) or decarboxylated and entering the Krebs cycle. However, the terms fast and slow better describe these processes because the glycolytic pathway itself does not depend directly on oxygen and because energy production occurs at a more rapid rate during fast compared to slow glycolysis (35).
Nanomaterials for Theranostics: Recent Advances and Future Challenges *
Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Eun-Kyung Lim, Taekhoon Kim, Soonmyung Paik, Seungjoo Haam, Yong-Min Huh, Kwangyeol Lee
In addition to the original and revised hallmarks described by Hanahan and Weinberg [29, 30], Luo and Elledge outlined the stress phenotypes of cancer, i.e., DNA damage/replication stress, proteotoxic stress, mitotic stress, metabolic stress, and oxidative stress [36]. For example, production of reactive oxygen species (ROS) is the defining characteristic of oxidative stress in cancer. ROS have been regarded as very sensitive stimuli while designing activatable nanotheranostic platforms [218, 219]. Moreover, ROS are highly linked to endogenous DNA damage events in cancer cells. Aerobic glycolysis, which is used for extensive proliferation, enables tumor cells to acidify their microenvironment (metabolic stress), leading to the escape from immune surveillance [164–168, 171]. Therefore, the acidic microenvironment of cancer cells provides excellent opportunities to optimally design multifunctional nanoplatforms for theranostic applications.
Whole-Body Regulation of Energy Expenditure, Exercise Fuel Selection, and Dietary Recommendations
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Oxidative Phosphorylation: At rest or with exercise below the respiratory threshold (∼60%–70% V˙O2max), aerobic glycolysis predominates. Here, pyruvic acid enters the mitochondria rather than being reduced to lactic acid and is converted into acetyl-CoA by the action of the pyruvate dehydrogenase complex, making the electron carrier nicotinamide adenine dinucleotide (NADH) available, as it is not needed to form lactic acid. The acetyl-CoA enters the citric acid cycle, where additional NADH and another electron carrier (FADH2), CO2, and a small amount of ATP (substrate phosphorylation) are formed. Ultimately, these carriers pass electrons along the electron transport chain (ETC), also located within the mitochondria, resulting in ATP synthesis, utilizing O2, and forming H2O as an end product. Since the 1960s this electron carrier oxidation coupling to ATP synthesis (chemiosmotic theory; 42) has been the prevailing explanation underlying how oxidative phosphorylation works, but data are accumulating that the torsional theory may more accurately explain the detail of this key step in oxidative metabolism (2, 45). Finally, aerobic metabolism predominates at rest and with low-to-moderate exercise intensities until the rate of pyruvic acid formation from accelerated glycolysis exceeds its maximal removal rate as acetyl-CoA into the citric acid cycle, at which point anaerobic glycolysis ramps up and muscle lactic acid production increases rapidly.
TKP, a Serine Protease from Trichosanthes kirilowii, Inhibits Cell Proliferation by Blocking Aerobic Glycolysis in Hepatocellular Carcinoma Cells
Published in Nutrition and Cancer, 2022
Aerobic glycolysis is defined as the seventh major feature of the tumor (31). Tumor cells mainly depend on aerobic glycolysis to gain energy. Even in the presence of oxygen, cancer cells prefer to consume higher amounts of glucose and convert glucose into lactate instead of performing oxidative phosphorylation (32). Aerobic glycolysis is crucial for cancer cell proliferation. Aerobic glycolysis provides cancer cells with energy and metabolic intermediates for inducing the rapid proliferation of cancer cells (17, 18). The present study indicated that TKP treatment significantly decreased the cell viability and colony formation rate of Bel-7402 and HepG2 cells, suggesting that TKP inhibits the proliferation of Bel-7402 and HepG2 cells. Moreover, we found that TKP markedly suppressed aerobic glycolysis, which was characterized by depressed glucose uptake, lactate production and the expression of aerobic glycolysis-related proteins including GLUT1, PDK, and LDHA. These results suggested that aerobic glycolysis is pivotal for TKP-induced inhibitory effects on the proliferation of Bel-7402 and HepG2 cells.
Fumarate hydratase as a therapeutic target in renal cancer
Published in Expert Opinion on Therapeutic Targets, 2020
Priyanka Kancherla, Michael Daneshvar, Rebecca A. Sager, Mehdi Mollapour, Gennady Bratslavsky
Lastly, as a result of the strict reliance on aerobic glycolysis, a particularly fascinating facet of ongoing research in this field involves targeting glycolysis. FH mutation, which completely removes the citric acid cycle as an energy production mechanism, represents a microcosm of the Warburg effect in cancer. One mechanism that has therefore been explored in order to target this is inhibition of LDHA. Further understanding of HLRCC can provide a greater understanding of the benefit of LDHA inhibition in cancers that are glycolysis dependent. Overall, there have been many advances to our understanding of the pathogenesis of HLRCC-associated RCC as a result of FH mutation. Consequently, there are many exciting and promising areas for the treatment of these tumors, and tumor-specific targeted therapy will become the norm in future treatment strategies.
Polychlorinated biphenyls promote cell survival through pyruvate kinase M2-dependent glycolysis in HeLa cells
Published in Toxicology Mechanisms and Methods, 2019
Yuting Zhang, Li Song, Zhuoyu Li
The aerobic glycolysis is the major metabolic pathway of cancer cells and crucial for cancer cell survival (Vander Heiden et al. 2009; Potter et al. 2016). To investigate whether PCBs affect the metabolism of HeLa cells, the relevant key indicators were measured. The results showed that treatment with 1 nM PCB126, PCB118, or PCB153 for 48 h significantly promotes aerobic glycolysis in HeLa cells, as manifested by the remarkable increase of glucose consumption and lactate production in culture medium (Figure 2(A,B)). Meanwhile, PCBs treatment also increased the expression of glycolysis-related proteins including glucose transporter-1 (GLUT1), lactate dehydrogenase (LDHA), and pyruvate dehydrogenase kinase (PDK) (Figure 3). These results indicated that PCBs could promote HeLa cell glycolysis.