How many acetyl coa per fatty acid

Possible Answers: Reduction of a carbon carbon double bond. Formation of a cis double bond between two carbons. Formation of a trans double bond between two carbons. Correct answer: Formation of a trans double bond between two carbons. Explanation : In the first step of beta oxidation the enzyme acyl-CoA dehydrogenase forms a trans-double bond between the two carbons at the site that will eventually be cleaved. Explanation : First, one must know what the products of one cycle of the beta oxidation pathway are.

Therefore: If taken into consideration, 2 ATP are needed to activate a fatty acid and allow it to enter into the mitochondria via the enzyme acyl-CoA synthetase. Therefore, the toTal net yield is For a quick reference, the following equations can be used: Where is number of carbons of an even numbered fatty acid chain.

Note: Palmitic acid is a saturated fatty acid containing sixteen carbon atoms. Correct answer:. Explanation : For each round of beta-oxidation, two carbon atoms are removed from the fatty acid chain. Possible Answers: 2 propionyl-CoA molecules. Correct answer: 2 acetyl-CoA molecules. Explanation : During beta oxidation of fatty acids, carbons are removed from the fatty acid chain two at a time.

Correct answer: 1 propionyl-CoA molecule and 1 acetyl-CoA molecule. Explanation : During beta-oxidation of fatty acids, carbons are removed from the fatty acid chain two at a time. During beta oxidation, what is the end product of a fatty acid with an odd number of carbons?

Possible Answers: Propionyl-CoA. Correct answer: Propionyl-CoA. Explanation : Fatty acids with an odd number of carbons are more common in plants and marine organisms than they are in mammals.

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Physiology Bethesda , 22 , Holloway, G. Acta Physiol. Oxford , , Tong, L. Acetyl-coenzyme A carboxylase: crucial metabolic enzyme and attractive target for drug discovery. Life Sci. Schreurs, M. Regulatory enzymes of mitochondrial beta-oxidation as targets for treatment of the metabolic syndrome. Adam, T. AMPK activation represses the human gene promoter of the cardiac isoform of acetyl-CoA carboxylase: Role of nuclear respiratory factor Schulz, H. Oxidation of fatty acids in eukaryotes.

Vance and J. Vance eds. Mazumder, R. Metabolism of propionic acid in animal tissues. Methylmalonyl co-enzyme A mutase holoenzyme. Kaziro, Y. Biotin and propionyl carboxylase. USA, 46 , Beck, W. Formation of succinate. Diedrich, M. The natural occurrence of unusual fatty-acids. Odd numbered fatty-acids. Nahrung , 34 , Regulation of fatty acid oxidation in heart. Eaton, S. Lipid Res. Huss, J. Nuclear receptor signaling and cardiac energetics. Dressel, U. Son, N.

Lin, J. Metabolic control through the PGC-1 family of transcription coactivators. The fate of the acetyl-CoA obtained from fatty acid oxidation depends on the needs of an organism. It may enter the citric acid cycle and be oxidized to produce energy, it may be used for the formation of water-soluble derivatives known as ketone bodies, or it may serve as the starting material for the synthesis of fatty acids.

For more information about the citric acid cycle, see Section In the liver, most of the acetyl-CoA obtained from fatty acid oxidation is oxidized by the citric acid cycle. Under normal conditions, the kidneys excrete about 20 mg of ketone bodies each day, and the blood levels are maintained at about 1 mg of ketone bodies per mL of blood. In starvation, diabetes mellitus, and certain other physiological conditions in which cells do not receive sufficient amounts of carbohydrate, the rate of fatty acid oxidation increases to provide energy.

This leads to an increase in the concentration of acetyl-CoA. The increased acetyl-CoA cannot be oxidized by the citric acid cycle because of a decrease in the concentration of oxaloacetate, which is diverted to glucose synthesis.

In response, the rate of ketone body formation in the liver increases further, to a level much higher than can be used by other tissues. The excess ketone bodies accumulate in the blood and the urine, a condition referred to as ketosis. When the acetone in the blood reaches the lungs, its volatility causes it to be expelled in the breath.

The sweet smell of acetone, a characteristic of ketosis, is frequently noticed on the breath of severely diabetic patients. Because two of the three kinds of ketone bodies are weak acids, their presence in the blood in excessive amounts overwhelms the blood buffers and causes a marked decrease in blood pH to 6.

This decrease in pH leads to a serious condition known as acidosis. One of the effects of acidosis is a decrease in the ability of hemoglobin to transport oxygen in the blood.

In moderate to severe acidosis, breathing becomes labored and very painful. The body also loses fluids and becomes dehydrated as the kidneys attempt to get rid of the acids by eliminating large quantities of water.