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Purpose We have previously shown that ATP maintenance is a promising way to prevent neuronal cell death, and that branched chain amino acids raised cellular ATP levels in cultured cells and antagonized cell death, as shown by the authors. In rodent models of retinal degeneration or glaucoma, BCAAs attenuated photoreceptor degeneration and retinal cell death. Methods of Measurement In HeLa cells under glycolysis and citric acid cycle inhibited conditions, the ATP concentration was determined. In HeLa or 661W cells transfected with enhanced green fluorescent protein-GLUTs, the intracellular function of GLUT1 and GLUT3 was observed. Endoplasmic reticulum stress or glycolysis inhibition have markedly elevated glucose uptake and recovered glucose uptake by BCAAs. paraphrasedoutput:. BCAAs increase ATP production by promoting glucose uptake by the introduction of glucose transporters translocation to the plasma membrane, promoting glucose uptake by increasing glucose uptake by promoting glucose uptake. These findings may help extend the clinical use of BCAAs in retinal neurodegenerative diseases, such as glaucoma and retinal degeneration.
Source link: https://europepmc.org/article/MED/35930269
Although glycolysis is the source of ATP in tumors, according to the Warburg effect, ATP levels do not differ between cancer cells grown in both presence and absence of glucose. We found that blocking fatty acid oxidation in the presence of glucose decreased ATP production in several cancer cells. Instead of metabolic reprogramming, we found that cancer cell proliferation mainly depends on metabolic nutrients and oxygen systemically delivered through the bloodstream rather than metabolic reprogramming. Tumor growth was 2-fold higher in mice fed a high-fat diet that caused obesity, according to a control/normal diet, but tumor growth was inhibited by threefolds in mice fed a calorie-balanced, low-fat diet. The difference in tumor growth between mice on low-fat and high-fat diets, according to this 5-fold difference in tumor formation, this fat-induced obesity promotes cancer formation, and tumor formation is largely dependent on fatty acids as the primary source of energy.
Source link: https://europepmc.org/article/MED/35868515
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