Biochem 13.1 Fatty Acid Metabolism Quiz

Chylomicron remnants and IDLs are enriched in cholesterol and cholesteryl esters after delivering triglycerides to target tissues.

High-density lipoproteins (HDLs) collect excess cholesterol from peripheral tissues and transport it back to the liver.

LDLs are even more enriched in cholesterol and serve to deliver cholesterol to peripheral tissues.

Triglycerides are broken down into free fatty acids and glycerol.

Free fatty acids can be further metabolized by β-oxidation, producing acetyl-CoA.

Glycerol, a product of triglyceride breakdown, can be converted into dihydroxyacetone phosphate (DHAP).

Fatty acid oxidation occurs primarily in mitochondria, where it produces acetyl-CoA.

Short-chain fatty acids and some medium-chain fatty acids can enter the mitochondrial matrix directly.

Acyl-CoA molecules are any hydrocarbon chain attached to coenzyme A through a thioester linkage.

Carnitine shuttle is a process used to transport long-chain fatty acids into the mitochondrial matrix for beta-oxidation.

Carnitine acyl transferase I (CAT I) is an enzyme located in the outer mitochondrial membrane that transfers the acyl group from coenzyme A to carnitine.

Acylcarnitine is a molecule formed when the acyl group is transferred from coenzyme A to carnitine.

CAT II, or carnitine acyl transferase II, is an enzyme inside the mitochondrial matrix that transfers the acyl group back onto coenzyme A.

Beta-oxidation is the process by which fatty acids are broken down into acetyl-CoA molecules in the mitochondrial matrix.

Acyl-CoA dehydrogenase catalyzes the first step of beta-oxidation, oxidizing the fatty acid chain and forming a trans double bond.

Trans-enoyl-CoA is an intermediate formed in the first step of beta-oxidation.

β-oxidation proceeds normally until the double bond is between carbons 3 and 4. Then, enoyl-CoA isomerase shifts the double bond from a cis position between carbons 3 and 4 to a trans position between carbons 2 and 3.

Acyl-CoA dehydrogenase introduces a double bond between carbons 2 and 3. However, the resulting conjugated double bonds prevent the molecule from fitting into enoyl-CoA hydratase's active site.

This process consumes NADPH, producing NADP+. Enoyl-CoA isomerase then acts on the new double bond to position it between carbons 2 and 3. β-oxidation then continues normally.

The consumption of NADPH is energetically equivalent to the consumption of NADH. This is because nicotinamide nucleotide transhydrogenase interconverts these molecules in the mitochondria.

In β-oxidation of unsaturated fatty acids with a double bond between odd-numbered and even-numbered carbons, one fewer FADH2 molecule is produced. This results in 1.5 fewer ATP molecules produced per fatty acid oxidized.

Enoyl-CoA isomerase converts the cis double bond between carbons 3 and 4 to a trans double bond between carbons 2 and 3.

The double bond between carbons 2 and 3 is the first step in β-oxidation of a saturated fatty acid and produces FADH2. However, in unsaturated fatty acids, the double bond is already present, so no oxidation-reduction reaction is needed.

Unlike saturated fatty acids, unsaturated fatty acids require specialized enzymes to process their existing double bonds during β-oxidation.

The liver produces glucose when the body is fasting.

Excess acetyl-CoA from beta-oxidation is converted into ketone bodies.

Ketone bodies are produced from acetyl-CoA and transported to other tissues for energy.

Acetoacetate can be directly exported or reduced to D-beta-hydroxybutyrate.

Ketone bodies indirectly transport NADH from the liver to other tissues.

Acetone is a byproduct of ketone body metabolism.

Ketone bodies are used as an energy source by tissues like muscles and heart.

High levels of acetone on the breath can indicate metabolic disorders, such as diabetes.

The synthesis of fatty acids from excess acetyl-CoA, primarily occurring when glucose is abundant.

The transport of acetyl-CoA from the mitochondria, where it's produced, to the cytosol, where fatty acid synthesis takes place, using citrate as a carrier molecule.

An enzyme responsible for splitting citrate into acetyl-CoA and oxaloacetate in the cytosol, allowing acetyl-CoA to be used for fatty acid synthesis.

The conversion of acetoacetate, a ketone body, into two molecules of acetyl-CoA, which can then enter the citric acid cycle to generate energy.

The process by which fatty acids are broken down into two-carbon units (acetyl-CoA) within the mitochondria.

The final step of beta-oxidation, where acetoacetyl-CoA is split into two acetyl-CoA molecules.

A molecule made of a hydrocarbon chain attached to coenzyme A, which is a key intermediate in both fatty acid oxidation and synthesis.

Fatty acid synthesis and oxidation occur in different compartments within the cell, with synthesis happening in the cytosol and oxidation in the mitochondrial matrix.

Malonyl-CoA, a key intermediate in fatty acid synthesis, inhibits carnitine acyltransferase I, preventing fatty acids from entering the mitochondria for β-oxidation.

Insulin stimulates fatty acid synthesis by activating acetyl-CoA carboxylase (ACC), which produces malonyl-CoA, while simultaneously inhibiting β-oxidation.

Glucagon triggers fatty acid oxidation by activating AMP-activated protein kinase (AMPK), which inactivates acetyl-CoA carboxylase (ACC), reducing malonyl-CoA production.

This regulatory mechanism prevents the simultaneous occurrence of fatty acid synthesis and oxidation, ensuring energy efficiency.

The process by which fatty acids are broken down into acetyl-CoA molecules in the mitochondrial matrix.

The enzyme that catalyzes the first step in β-oxidation, oxidizing the fatty acid chain and forming a trans double bond.