The way through which high levels of cytoplasmic NADH (nicotinamide adenine dinucleotide reduced) provide a source of NADPH (nicotinamide adenine dinucleotide phosphate) for the synthesis of fatty acid. Introduction: Metabolic reactions are of two different types, namely, anabolic and catabolic reactions. Both, anabolic and catabolic reactions require oxidizing and reducing agents. NADH acts as a significant reducing agent in cellular catabolism and NADPH plays an important role in anabolic reactions.

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Chapter 9, Problem 38SA

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The way through which high levels of cytoplasmic NADH (nicotinamide adenine dinucleotide reduced) provide a source of NADPH (nicotinamide adenine dinucleotide phosphate) for the synthesis of fatty acid.

Introduction:

Metabolic reactions are of two different types, namely, anabolic and catabolic reactions. Both, anabolic and catabolic reactions require oxidizing and reducing agents. NADH acts as a significant reducing agent in cellular catabolism and NADPH plays an important role in anabolic reactions.

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One consequence 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 aldehyde dehydrogenase to yield acetate and 2 NADH. Acetate is then transported into the mitochondrion, where it is converted to acetyl-CoA and metabolized in the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels of NADH cause metabolic abnormalities, one of which is high levels of fatty acid synthesis. Fatty acid synthesis, also a cytoplasmic process, uses acetyl-CoA as a substrate and NADPH as a reducing agent. Speculate about how a high level of cytoplasmic NADH provides a source of NADPH for fatty acid synthesis.

One of the consequences of ethanol addiction is fattyliver disease, an illness in which liver cells accumulatetriacylglycerols, the esters derived from glycerol and fattyacids. Ethanol is oxidized in the cytoplasm of liver cells byalcohol dehydrogenase and aldehyde dehydrogenase to yieldacetate and 2 NADH. Acetate is then transported into themitochondrion, where it is converted to acetyl-CoA andmetabolized by the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels ofNADH cause metabolic abnormalities, one of which is highlevels of fatty acid synthesis. Fatty acid synthesis, also acytoplasmic process, uses acetyl-CoA as a substrate andNADPH as a reducing agent. Determine how a high level ofcytoplasmic NADH provides a source of NADPH for fattyacid synthesis.

Which of the following is most likely to cause accumulation of acetyl CoA? Group of answer choices There is not enough oxaloacetate present to run the citric acid cycle Increase activity of pyruvate dehydrogenase kinase Increased fatty acid synthesis Increased citrate synthase activity When fluoroacetate (an analog of acetate) is added to the mitochondria, it causes build up of fluorocitrate. Which of the following is most likely to be true? Group of answer choices Fluoroacetate cannot be converted to fluoroacetyl CoA Fluoroacetyl CoA cannot be combined with oxaloacetate to enter the citric acid cycle Addition of fluoroacetate will cause an increase in isocitrate Aconitase cannot use fluorocitrate as a substrate