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One of the consequences of ethanol addiction is fatty liver disease, an illness in which liver cells accumulate large amounts of triacylglycerols, the esters derived from glycerol and fatty acids. Ethanol is oxidized in the cytoplasm of liver cells by alcohol dehydrogenase and
C. How would excess G6P concentration contribute to the reducing potential required for fatty acid synthesis? Excess G6P usually means that glycolysis is not occurring and NADH is not being used up.
D. How does acetate stimulate the rate of citrate formation based on enzyme kinetic?
E. How would the concentration of citrate in the mitochondria increase if the rate of isocitrate dehydrogenase rate were inhibited
The enzyme citrate synthase exists in nearly all living cells and stands as a pace-maker enzyme in the citric acid cycle. Citrate synthase is present within eukaryotic cells in the mitochondrial matrix, but is encoded by nuclear DNA rather than mitochondrial. It is synthesized using cytoplasmic ribosomes, then transported to the mitochondrial matrix.
Citrate synthase catalyses the condensation reaction of two-carbon acetate residue from acetyl coenzyme A and a molecule of four-carbon oxaloacetate to form the six-carbon citrate:
acetyl-CoA + oxaloacetate + H2O → citrate + CoA-SH
In Tricarboxylic acid cycle (TCA cycle) acetate is converted into Acetyl CoA with the utilization of ATP and release CoA. This Acetyl CoA further converts into citrate with the liberation of water molecule.
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