Catabolism of Fatty Acids Flashcards

Flashcards for Catabolism of Fatty Acids

Formation of Acyl-CoA

Addition of a phosphate group from ATP forming acyl-adenylate, which binds to acyl-CoA synthetase and coenzyme A.

Synthesis of Acyl-Carnitine

Enzyme carnitine acyl-transferase-I attaches a carnitine molecule to acyl-CoA, forming acyl-carnitine and freeing coenzyme A.

Formation of Acyl-CoA (mitochondrial matrix)

Enzyme carnitine acyl-transferase-II acts, uniting a CoA and liberating carnitine, to regenerate acyl-CoA in the mitochondrial matrix.

β-oxidation of saturated fatty acids

Degradative process of fatty acids through successive oxidations, releasing acetyl-CoA molecules.

Dehydrogenation (β-oxidation)

Creates a trans configuration double bond, resulting in trans-Δ2-enoyl-CoA.

Number of cycles in β-oxidation

The number of cycles is determined by the formula (number of Carbons / 2) – 1.

β-oxidation of monounsaturated fatty acids

Oxidation of monounsaturated fatty acids requires an isomerase because enoyl-CoA enzyme substrates must be trans isomers.

Processing propionyl-CoA

Requires transformation into succinyl-CoA, consuming one ATP and preventing the production of two NADH molecules from the beginning of the Krebs cycle.

Acetyl-CoA carboxylase (ACC)

First enzyme in fatty acid synthesis.

Carnitine acyl-transferase-I

Enzyme responsible for introducing fatty acids into the mitochondrial matrix.

Effect of insulin on ACC

After absorbing carbohydrates from the diet, the concentration of glucose in the blood increases, and therefore insulin is released, which activates a phosphatase that dephosphorylates ACC, activating it.

Malonyl-CoA

Inhibits carnitine acyltransferase I, preventing fatty acids from entering the mitochondria.

Effect of glucagon on ACC

When the glucose concentration in the blood decreases, glucagon is released, which activates the kinase PKA. PKA phosphorylates ACC, inactivating it.