Eicosanoids and Prostaglandin Synthesis

A group of 20-carbon compounds derived from arachidonic acid.

A specific type of eicosanoid synthesized via the cyclooxygenase (COX) pathway that plays a key role in inflammation.

Drugs like aspirin and ibuprofen that work by inhibiting cyclooxygenase (COX) enzymes, thus reducing inflammation, pain, and fever.

A key enzyme involved in prostaglandin synthesis, found in two forms: COX-1 and COX-2.

A process where fatty acids are broken down to generate energy, primarily occurring in the mitochondria.

The production of fatty acids from smaller building blocks.

Enzymes that activate phospholipase (PL), leading to the release of arachidonic acid, a precursor for eicosanoid production.

Steroids inhibit the release of arachidonic acid from membranes, thus reducing eicosanoid production.

The process of breaking down triacylglycerols (TAGs) in adipose tissue to release fatty acids and glycerol. It's a key process for providing energy during fasting or prolonged exercise.

An enzyme activated by hormones like glucagon and epinephrine, initiating the breakdown of TAGs in adipose tissue.

A protein that activates ATGL and is involved in the breakdown of TAGs.

A lipase that breaks down TAGs into diacylglycerol (DAG), the first step in lipolysis.

An enzyme that converts long-chain fatty acids into their activated form (fatty acyl CoA) in the cytosol. This is essential for the transport of fatty acids into mitochondria for beta oxidation.

A protein that binds to fatty acids in the blood and transports them to various tissues.

The inner mitochondrial membrane is impermeable to CoA, requiring special carriers to transport activated fatty acids (fatty acyl CoA) into the mitochondrial matrix for beta oxidation.

A process that shuttles long-chain fatty acids into the mitochondria, where they can be broken down for energy production. It involves three steps: acyl group transfer from CoA to carnitine, transport of acylcarnitine into the mitochondrial matrix, and transfer of the acyl group back to CoA within the mitochondria.

An enzyme located on the outer mitochondrial membrane that catalyzes the first step of the carnitine shuttle, transferring an acyl group from CoA to carnitine.

A molecule that acts as a carrier for long-chain fatty acids across the mitochondrial membrane.

An enzyme located on the inner mitochondrial membrane that catalyzes the final step of the carnitine shuttle, transferring the acyl group back to CoA in the mitochondrial matrix.

A molecule that inhibits CPT-I, thus preventing the entry of long-chain fatty acids into the mitochondria. Its presence indicates sufficient energy from other sources.

A condition caused by a decreased ability to utilize long-chain fatty acids as fuel. It can be primary due to defects in a membrane transporter or secondary due to defects in fatty acid oxidation.

A form of carnitine deficiency caused by defects in a membrane transporter that normally transports carnitine into cells.

A form of carnitine deficiency that occurs due to defects in fatty acid oxidation, resulting in the accumulation of acylcarnitines and decreased carnitine availability.

An enzyme involved in the rate-limiting step of de novo fatty acid synthesis, catalyzing the carboxylation of acetyl-CoA to malonyl-CoA.

A process that breaks down fatty acids into acetyl-CoA units, generating energy for the cell.

These are essential for membrane structure, acting as building blocks for cell membranes.

This shuttle moves acetyl-CoA from the mitochondria to the cytoplasm, where it's used for fatty acid synthesis.

The process of generating new fatty acids from smaller building blocks.

A class of enzymes that break down triacylglycerols (fats) into fatty acids and glycerol.

A complex process that requires specific enzymes to convert unsaturated fatty acids into usable forms for beta-oxidation.

An enzyme that converts pyruvate to lactate, generating NADH and contributing to the production of acetyl-CoA.

Short chain fatty acids (SCFAs) and medium-chain fatty acids (MCFAs) can directly cross the inner mitochondrial membrane via simple or facilitated diffusion. They don't require carnitine shuttling like longer fatty acids.

The first step in beta-oxidation involves the removal of two hydrogen atoms from the fatty acyl CoA molecule, producing a trans enoyl CoA and reducing FAD to FADH2.

In the second step of beta-oxidation, water is added across the double bond of the trans enoyl CoA, forming a beta-hydroxy fatty acyl CoA.

The third step of beta-oxidation involves the oxidation of the beta-hydroxy fatty acyl CoA by NAD+, generating a beta-keto fatty acyl CoA and reducing NAD+ to NADH.

In the fourth and final step, the bond between the alpha and beta carbon atoms is cleaved, resulting in the production of acetyl CoA and a fatty acyl CoA that is two carbons shorter.

When metabolizing odd-chain fatty acids, beta-oxidation continues until a 3-carbon unit, propionyl CoA, is produced.

Propionyl CoA is first carboxylated to D-methyl malonyl CoA, then isomerized to L-methyl malonyl CoA, and finally rearranged to succinyl CoA, which can enter the TCA cycle.

Succinyl CoA, formed from propionyl CoA, can enter the TCA cycle and ultimately be converted to oxaloacetate, which can be used for gluconeogenesis.