This step controls the metabolic flux of beta oxidation.

Octanoyl-coenzyme A is the endpoint of beta oxidation in peroxisomes.

This undergoes reduction and three rounds of beta oxidation to form jasmonic acid.

Once the fatty acid is inside the mitochondrial matrix, Beta Oxidation can begin.

These enzymes are those associated with ether-lipid synthesis or the beta oxidation of certain fatty acids.

This gene encodes an enzyme operative in the beta oxidation system of the peroxisomes.

The compound undergoes beta oxidation, forming one or more molecules of acetyl-CoA.

They are consumed by mitochondria to produce ATP through beta oxidation.

The encoded protein catalyzes the last step of the mitochondrial fatty acid beta oxidation spiral.

Mitochondrial trifunctional protein is a protein which catalyzes several reactions in beta oxidation.

In liver, pristanic acid is degraded by peroxisomal beta oxidation to propionyl-CoA.

They must first undergo beta oxidation in the mitochondria (mostly of skeletal muscle, cardiac muscle, and liver cells).

Beta Oxidation of Fatty Acids.

These processes include glycolysis, purine salvage, beta oxidation of fatty acids, and ether lipid synthesis.

This enzyme is required for production of dicarboxylic acids by industrial Candida yeast, which have nonfunctional beta oxidation pathways.

ETFA participates in catalyzing the initial step of the mitochondrial fatty acid beta oxidation.

Fatty acids can be oxidized again to make dicarboxylic species that join with coenzyme A and enter the beta oxidation pathway in the peroxisome.

(Propionyl-CoA is released as a result of beta oxidation when the beta carbon is substituted)

Acyl-carnitines are involved in the transport and metabolism of fatty acids in and out of mitochondria, where they undergo beta oxidation.

Beta oxidation is the metabolic process by which fatty acids are broken down in the mitochondria and/or in peroxisomes to generate acetyl-CoA.

Since propanoic acid has three carbons, propionyl-CoA can directly enter neither beta oxidation nor the citric acid cycles.

As for example 2,3-dinor-6-keto Prostaglandin F1α is produced by beta oxidation of the parent compound 6-keto Prostaglandin F1α.

It is now considered more likely that DHA is biosynthesized via a C24 intermediate followed by beta oxidation in peroxisomes.

This gene encodes an accessory enzyme that participates in the beta oxidation and metabolism of polyunsaturated fatty enoyl-CoA esters.

The glycerol enters glycolysis and the fatty acids are broken down by beta oxidation to release acetyl-CoA, which then is fed into the citric acid cycle.

It of course, does this through a completely different metabolic pathway called beta-oxidation.

Most of the body is able to use fatty acids as an alternative source of energy in a process called beta-oxidation.

Fatty acids can also be broken down to acetyl-CoA by beta-oxidation.

Fatty acid beta-oxidation provides energy after the body has used up its stores of glucose and glycogen.

It is formed as a product of beta-oxidation of odd-chain fatty acids.

This enzyme functions in the auxiliary step of the fatty acid beta-oxidation pathway.

The first stage of fatty acid catabolism is Beta-Oxidation.

The carnitine palmitoyltransferase system is an essential step in the beta-oxidation of long chain fatty acids.

This enzyme catalyses a hydration step in peroxisomal beta-oxidation.

A major function of the peroxisome is the breakdown of very long chain fatty acids through beta-oxidation.

MCPA acts to inhibit the beta-oxidation of fatty acids in two ways.

One of the products of beta-oxidation is acetyl-CoA, which can be further used in the citric acid cycle.

Inhibition of beta-oxidation of fatty acids, however, also depletes a necessary cofactor for gluconeogenesis.

In plants and insects propionyl-CoA is metabolized to acetate in a very different way, similar to beta-oxidation.

It is also synthesized from propionyl CoA, the odd-numbered fatty acid, which cannot undergo beta-oxidation.

Carnitine is essential for the transport of activated fatty acids across the mitochondrial membrane during mitochondrial beta-oxidation.

Leptospira are aerobes whose major carbon and energy source during in vitro growth is long-chain fatty acids, which are metabolized by beta-oxidation.

Fatty Acid Catabolism or Beta-Oxidation:

Step 1 of Beta-Oxidation: Long chain fatty acid is dehydrogenated to create a trans double bond between C2 and C3.

Beta-oxidation of unsaturated fatty acids changes the ATP yield due to the requirement of two possible additional enzymes.

Trimetazidine inhibits beta-oxidation of fatty acids by blocking long-chain 3-ketoacyl-CoA thiolase, which enhances glucose oxidation.

Women have higher ALA conversion efficiency than men, which is presumed to be due to the lower rate of use of dietary ALA for beta-oxidation.

The alpha subunit of fatty acid oxidation complex, a multi-enzyme complex that catalyses the last three reactions in the fatty acid beta-oxidation cycle.

Malonyl-CoA is a highly-regulated molecule in fatty acid synthesis; as such, it inhibits the rate-limiting step in beta-oxidation of fatty acids.

This gene encodes the beta subunit of the mitochondrial trifunctional protein, which catalyzes the last three steps of mitochondrial beta-oxidation of long chain fatty acids.