How is malonyl-CoA produced?

Malonyl-CoA is formed by carboxylating acetyl-CoA using the enzyme acetyl-CoA carboxylase. One molecule of acetyl-CoA joins with a molecule of bicarbonate, requiring energy rendered from ATP. MCAT serves to transfer malonate from malonyl-CoA to the terminal thiol of holo-acyl carrier protein (ACP).

What is the substrate for malonyl-CoA synthesis?

Malonyl-CoA is a key intermediary metabolite in fatty acid synthesis. In de novo fatty acid synthesis, malonyl-coenzyme A (CoA) is the substrate that provides the primary carbon source for the formation of palmitate (C16) catalyzed by fatty acid synthase (FASN).

What is ACC in fatty acid synthesis?

ACC is a multi-subunit enzyme in most prokaryotes and in the chloroplasts of most plants and algae, whereas it is a large, multi-domain enzyme in the cytoplasm of most eukaryotes. The most important function of ACC is to provide the malonyl-CoA substrate for the biosynthesis of fatty acids.

What metabolite is the source of malonyl-CoA synthesis?

IMPORTANCE ACCase is responsible for carboxylation of acetyl-CoA to produce malonyl-CoA, which is a crucial step in the control of fatty acid metabolism.

What pathway does malonyl-CoA inhibit?

Malonyl CoA is an inhibitor of CPT1, the enzyme that controls the transfer of long-chain fatty acyl (LCFA) CoA molecules from the cytosol into mitochondria where they are oxidized.

What happens to malonyl-CoA in fatty acid synthesis?

The fall in malonyl-CoA stops fatty acid synthesis and activates CPT1 and ketogenesis (8). We also showed that the malonyl-CoA system functions in skeletal and cardiac muscle, although these tissues do not make ketones (9). Regulation of malonyl-CoA determines the switch between fatty acid synthesis and oxidation.

What happens to malonyl-CoA?

What does malonyl-CoA do?

Malonyl-CoA is an inhibitor of carnitine palmitoyltransferase I, the enzyme that controls the oxidation of fatty acids by regulating their transfer into the mitochondria. Despite this, knowledge of how malonyl-CoA levels are regulated in skeletal muscle, the major site of fatty acid oxidation, is limited.

How does palmitoyl CoA inhibit ACC?

Skeletal muscle ACC is more potently inhibited by palmitoyl-CoA after having been phosphorylated by AMPK. This may contribute to low-muscle malonyl-CoA values and increasing fatty acid oxidation rates during long-term exercise when plasma fatty acid concentrations are elevated.