Coenzyme A and Acetyl-CoA: The Carrier and the Fuel Hub of Metabolism

Short answer

• Coenzyme A, usually shortened to CoA, is a helper molecule that carries carbon groups, called acyl groups, from one reaction to another. It is not an enzyme and it does not make energy on its own.
• Acetyl-CoA is CoA carrying a two carbon acetyl group. It forms when CoA picks up that acetyl group, most famously from pyruvate after glycolysis, from fatty acids during beta-oxidation, and from some amino acids.
• Acetyl-CoA is a crossroads of metabolism. In mitochondria it delivers its acetyl group to the citric acid cycle for energy extraction and, in liver cells, to ketone body synthesis, and in the cytosol it supplies the starting material for fatty acid synthesis, cholesterol synthesis, acetylcholine, and protein acetylation.
• CoA is built from vitamin B5, also called pantothenic acid, plus a nucleotide portion related to adenosine diphosphate and a sulfur containing arm that ends in a thiol group. The acetyl group attaches to that thiol group through a high energy thioester bond.
• The two names describe one carrier in two states: empty CoA, and loaded CoA, which is acetyl-CoA. When the acetyl group is handed off, CoA is freed to carry another group.

What the Phrase “Coenzyme A Acetyl CoA” Actually Means

Searchers who type “coenzyme a acetyl coa” are usually trying to untangle two names that always appear together. The confusion is understandable, because the two molecules differ by a single small group, and textbooks often introduce them in the same sentence. The relationship is simple once it is stated plainly: coenzyme A is the carrier, and acetyl-CoA is the carrier with its most famous cargo loaded.

Think of CoA as a delivery handle. On its own it carries nothing, but its shape lets enzymes grab it, load a carbon fragment onto it, move that fragment to the next reaction, and unload it. The acetyl group is a two carbon fragment with the formula CH3CO. When that fragment is attached to CoA, the resulting molecule is acetyl-CoA. When the acetyl group is removed, CoA is free again. The cell therefore does not need a separate transport system for every two carbon unit. It reuses the same carrier thousands of times.

That reuse is why CoA appears in so many pathways. Succinyl-CoA carries a four carbon succinyl group inside the citric acid cycle, malonyl-CoA carries a three carbon malonyl group in fatty acid synthesis, and acyl-CoA is the general name for CoA carrying any acyl group. Acetyl-CoA is simply the most common and most central member of that family.

What Is Coenzyme A?

Coenzyme A is a small, water soluble coenzyme found in every living cell. A coenzyme is a nonprotein helper molecule that an enzyme needs in order to do its job. Enzymes are proteins that speed up chemical reactions. Coenzymes are not enzymes themselves. They assist enzymes, often by carrying a chemical group or an electron from one reaction to another.

CoA works by activation. A carbon group attached to CoA is chemically more useful than the same group floating free, because the bond that holds it is reactive and its energy can help drive the next reaction. Enzymes can therefore take a group from CoA and attach it to another molecule more easily than they could handle the free group. In that sense CoA does not just transport its cargo. It primes its cargo for use.

The cell makes CoA from vitamin B5, pantothenic acid. That is the reason pantothenic acid is classed as an essential vitamin in humans: the body cannot make it, so it must come from food, and CoA synthesis depends on it. This article makes no dietary recommendation.

The Structure of CoA, in Plain Terms

CoA has three recognizable parts, and each part explains something about how it works.

First, there is a nucleotide portion built around adenosine diphosphate, or ADP. This part gives CoA a shape that enzymes recognize and grip. It is the same kind of adenine, ribose, and phosphate architecture found in ATP, but with two phosphate groups rather than three, and with an extra phosphate attached at the 3 prime position of the ribose sugar. That 3 prime phosphate is a distinctive fingerprint of CoA, and it helps enzymes distinguish CoA from other ADP containing molecules.

Second, there is pantothenic acid, vitamin B5. Pantothenic acid itself is made of two smaller pieces, pantoic acid and beta-alanine, joined by an amide bond. In CoA, pantothenic acid forms the middle arm of the molecule, linking the nucleotide portion to the business end.

Third, there is the business end: a beta-mercaptoethylamine group, also described as a cysteamine group, which ends in a sulfur hydrogen group called a thiol, written as SH. This thiol is the attachment point. When an acyl group binds to the sulfur atom of the thiol, the result is a thioester bond. That bond is the key to everything CoA does.

The thioester bond is often called a high energy bond, which needs a careful explanation. It does not store energy the way a battery stores charge. It is a reactive bond whose breaking releases a useful amount of free energy, roughly 31 kilojoules per mole for the acetyl-CoA thioester bond. That released energy helps drive the reaction that follows, which is why acetyl-CoA can hand its acetyl group to another molecule and why enzymes prefer to work with CoA bound groups rather than free acids. When the acetyl group is transferred, the thioester bond breaks and free CoA, sometimes written CoA-SH to show its free thiol, is released for reuse.

How Acetyl-CoA Forms

Acetyl-CoA is not one fixed product of one reaction. It is a molecule the cell makes by several routes, depending on which fuel is available. The routes differ, but the endpoint is the same: a two carbon acetyl group attached to CoA through a thioester bond.

From Pyruvate: the Link Between Glycolysis and the Citric Acid Cycle

The best known route starts with glucose. In glycolysis, which takes place in the cytosol, one glucose molecule is split into two molecules of pyruvate, each with three carbons. Pyruvate cannot enter the citric acid cycle directly. It must first be converted, and that conversion is where CoA enters the story.

In eukaryotic cells, pyruvate is transported into the mitochondria, the cell structures where aerobic respiration takes place. There, in the mitochondrial matrix, a large multienzyme complex called the pyruvate dehydrogenase complex converts pyruvate to acetyl-CoA in three steps. First, a carboxyl group is removed from pyruvate, releasing a molecule of carbon dioxide. This removes one of the three carbons of pyruvate. Second, the remaining two carbon fragment is oxidized to an acetyl group, and the electrons released are picked up by NAD+, forming NADH. Third, the acetyl group is transferred to CoA, producing acetyl-CoA.

That sequence matters for carbon accounting. Each glucose molecule produces two pyruvates, so this step runs twice per glucose and releases two carbon dioxide molecules, accounting for two of the six carbons of the original glucose. The other four carbons are released as carbon dioxide later, during turns of the citric acid cycle. The NADH formed here carries high energy electrons onward to the electron transport chain, where they help produce ATP.

From Fatty Acids: Beta-Oxidation

The second major route is the breakdown of fatty acids, called beta-oxidation. Fatty acids are long carbon chains, and beta-oxidation shortens them two carbons at a time. In each round, enzymes cut a two carbon unit from the chain and attach it to CoA, producing one molecule of acetyl-CoA, plus NADH and FADH2, which are electron carriers. A 16 carbon fatty acid such as palmitate therefore yields eight acetyl-CoA molecules after repeated rounds. This is why fatty acids are such energy dense fuels: a single long chain feeds many acetyl-CoA molecules into the citric acid cycle.

Mitochondrial beta-oxidation supplies acetyl-CoA for two different purposes depending on the tissue. In skeletal and cardiac muscle, that acetyl-CoA feeds the citric acid cycle and supports ATP production for contraction. In liver cells, the same acetyl-CoA can instead be directed toward ketone body synthesis when glucose is scarce.

From Amino Acids and Acetate

Some amino acids can also feed into acetyl-CoA. When proteins are broken down, certain amino acids are converted through their own pathways into acetyl-CoA or into citric acid cycle intermediates. These are called ketogenic amino acids when their breakdown yields acetyl-CoA or acetoacetate. The details differ by amino acid, but the principle is the same: the cell routes surplus carbon skeletons into the shared acetyl-CoA pool rather than wasting them.

A fourth route starts from acetate itself. An enzyme called acetate-CoA ligase, also known as acetyl-CoA synthetase, joins acetate to CoA using energy from ATP, producing acetyl-CoA directly. This route also operates in the cytosol and nucleus, where it can supply acetyl-CoA for protein acetylation without involving mitochondria at all.

Acetyl-CoA in the Citric Acid Cycle

The citric acid cycle, also called the tricarboxylic acid cycle or Krebs cycle, is the main energy extracting pathway that acetyl-CoA feeds. It takes place in the mitochondrial matrix in eukaryotes. The cycle is a closed loop, not a straight line: its last step regenerates the molecule used in its first step, so it can keep turning as long as acetyl-CoA and other reactants are supplied.

The entry step is a condensation reaction. The two carbon acetyl group of acetyl-CoA joins a four carbon molecule called oxaloacetate to form a six carbon molecule called citrate. The enzyme is citrate synthase. In this step CoA is released, its thiol freed, so it can diffuse away and pick up another acetyl group. That release and reuse is the carrier cycle in miniature: loaded CoA arrives, unloads, and leaves empty.

The rest of the cycle processes citrate through a series of steps. Citrate is converted to its isomer isocitrate, which is oxidized to alpha-ketoglutarate, a five carbon molecule, releasing one carbon dioxide and reducing NAD+ to NADH. Alpha-ketoglutarate is then oxidatively decarboxylated to succinyl-CoA, releasing a second carbon dioxide and another NADH. Note that CoA appears here again, this time carrying a succinyl group rather than an acetyl group. Succinyl-CoA is converted to succinate, producing one GTP or ATP by substrate level phosphorylation depending on the tissue. Succinate is oxidized to fumarate, reducing FAD to FADH2. Fumarate is hydrated to malate, and malate is oxidized back to oxaloacetate, producing a third NADH and closing the loop.

Counted per turn of the cycle, meaning per acetyl group fed in, the yield is two carbon dioxide molecules, three NADH molecules, one FADH2 molecule, and one ATP or GTP. The cycle itself produces very little ATP directly and does not directly consume oxygen. Its main energy output is in the reduced carriers NADH and FADH2, which carry electrons to the electron transport chain. There, in the presence of oxygen, those electrons drive the production of most of the ATP of aerobic respiration. If that electron transfer stops, the oxidation steps of the cycle also stop, which is why the citric acid cycle is classed as an aerobic pathway even though oxygen does not appear in its own reactions.

Two regulation points deserve attention, because they show acetyl-CoA acting as a signal as well as a substrate. The entry step is controlled by negative feedback: when ATP levels are high, the rate of citrate formation falls, and when ATP is in short supply, the rate rises. High levels of NADH also inhibit the cycle, because the cycle needs a supply of NAD+ to accept electrons. The cell therefore matches the cycle to its energy state rather than running it at full speed regardless of need.

Where Acetyl-CoA Lives: Compartments Matter

One of the most important subtleties of acetyl-CoA biology is that the cell keeps separate pools of it in separate compartments, and those pools do different jobs. Acetyl-CoA cannot freely cross the inner mitochondrial membrane. That barrier is not a flaw. It is how the cell prevents its energy burning pool and its building pool from competing with each other.

Mitochondrial acetyl-CoA is the energy pool, made there by the pyruvate dehydrogenase complex and by beta-oxidation, and consumed there by the citric acid cycle and by ketone body synthesis. Cytosolic acetyl-CoA is the building pool, supplying fatty acid synthesis, cholesterol synthesis, and protein acetylation. Nuclear acetyl-CoA, a smaller pool, supplies histone acetylation, which affects gene expression.

Because mitochondrial acetyl-CoA cannot cross the membrane directly, the cell uses a shuttle to move its carbon to the cytosol. Inside the mitochondrion, acetyl-CoA condenses with oxaloacetate to form citrate. That citrate is exported across the mitochondrial membrane into the cytosol, where an enzyme called ATP-citrate lyase splits it back into acetyl-CoA and oxaloacetate. The cytosol thereby gains acetyl-CoA without any acetyl-CoA molecule itself crossing the membrane. This citrate shuttle is the bridge between energy metabolism and fat synthesis: glucose carbon travels from pyruvate to mitochondrial acetyl-CoA to citrate to cytosolic acetyl-CoA to fatty acids.

Acetyl-CoA and Fatty Acid Synthesis

Fatty acid synthesis is the mirror image of beta-oxidation. Beta-oxidation breaks fatty acids into acetyl-CoA units. Synthesis builds fatty acids from acetyl-CoA units. The two pathways are kept separate, in different compartments and under different regulation, so the cell does not run both at full speed at the same time in a futile loop.

Synthesis takes place in the cytosol, mainly in liver and adipose tissue. Its first committed step is catalyzed by acetyl-CoA carboxylase, which converts acetyl-CoA to malonyl-CoA using ATP and bicarbonate, with the vitamin biotin as a carrier for the carboxyl group. Calling it the first committed step means that once acetyl-CoA is converted to malonyl-CoA, it is committed to fatty acid synthesis rather than to other uses, which is why acetyl-CoA carboxylase is a major control point.

The fatty acid synthase complex then builds the chain. It starts with one acetyl group as a primer and repeatedly adds two carbon units donated by malonyl-CoA, each round followed by reduction and dehydration steps that leave a saturated chain two carbons longer. The process repeats until the chain reaches 16 carbons, producing palmitate, the standard end product of de novo fatty acid synthesis. Palmitate can then be lengthened further or desaturated, or stored as triglyceride.

The regulatory logic is worth stating plainly. When energy is abundant, citrate leaves the mitochondrion, cytosolic acetyl-CoA rises, acetyl-CoA carboxylase is active, and fatty acid synthesis runs. When energy is scarce, the cell instead burns fatty acids by beta-oxidation, producing mitochondrial acetyl-CoA for the citric acid cycle. Malonyl-CoA reinforces this switch: it inhibits the transport of fatty acids into mitochondria for oxidation, so synthesis and oxidation do not compete directly. Acetyl-CoA sits at the center of that switch, both as the raw material and as the signal.

Other Pathways Fed by Acetyl-CoA

Energy and fat synthesis are the headline roles, but acetyl-CoA feeds several other pathways that explain why it is described as a central metabolite rather than just a fuel intermediate.

Ketone Bodies

When acetyl-CoA production in the liver exceeds the capacity of the citric acid cycle to oxidize it, the excess is directed toward ketogenesis. This happens during prolonged fasting or carbohydrate deprivation, when oxaloacetate is in limited supply because it is being used for glucose synthesis. Two molecules of acetyl-CoA condense to form acetoacetyl-CoA, which is then converted to HMG-CoA, short for 3-hydroxy-3-methylglutaryl-CoA, and then cleaved to acetoacetate. Acetoacetate can be reduced to D-beta-hydroxybutyrate or decarboxylated to acetone. Acetoacetate and D-beta-hydroxybutyrate are released into the blood and serve as alternative fuels for extrahepatic tissues, particularly the brain, heart, and skeletal muscle. The liver itself cannot use ketone bodies for fuel, because it lacks succinyl-CoA:acetoacetate-CoA transferase (thiophorase), the enzyme that converts acetoacetate back to acetyl-CoA, so ketone bodies are an export product, not a local fuel.

Cholesterol and Steroid Synthesis

Cytosolic acetyl-CoA also feeds the mevalonate pathway, which makes cholesterol. Two acetyl-CoA molecules condense to acetoacetyl-CoA, which then combines with a third acetyl-CoA to form HMG-CoA. HMG-CoA is then reduced to mevalonate, in the rate limiting step of cholesterol synthesis, and mevalonate is processed through a series of steps to cholesterol. Cholesterol is used as a structural component of cell membranes and as the starting material for steroid hormones, bile salts, and vitamin D.

Acetylcholine

Acetyl-CoA is also the acetyl donor for the neurotransmitter acetylcholine. In cholinergic neurons, the enzyme choline acetyltransferase transfers the acetyl group from acetyl-CoA to choline, producing acetylcholine and free CoA. The acetyl group in the neurotransmitter therefore comes, ultimately, from the same acetyl-CoA pool that feeds energy metabolism, although the neuron maintains its own local supply through ATP-citrate lyase and other enzymes.

Protein Acetylation and Gene Regulation

Acetyl-CoA is the donor for protein acetylation, a modification in which an acetyl group is attached to a protein, most famously to lysine residues on histones. Histones are the proteins around which DNA is wrapped, and acetylation of histones changes how tightly DNA is packaged and therefore how accessible genes are for expression. Because histone acetylation depends on the local supply of acetyl-CoA, changes in metabolism can influence gene expression. The broad point is simpler: acetyl-CoA is not only a fuel and a building block. It is also a chemical messenger whose availability shapes which proteins are modified and which genes are switched on.

Regulation by Acetyl-CoA Itself

Acetyl-CoA also regulates its own production. It activates pyruvate dehydrogenase kinase, an enzyme that switches off the pyruvate dehydrogenase complex, and it activates pyruvate carboxylase, an enzyme that replenishes oxaloacetate. The ratio of acetyl-CoA to free CoA therefore acts as a gauge of the cell’s fuel state. When acetyl-CoA is high relative to CoA, the cell has plenty of two carbon fuel, so it slows further pyruvate conversion and favors storage pathways. When the ratio falls, the brake lifts and pyruvate conversion resumes.

CoA, Acetyl-CoA, and Other Acyl-CoAs at a Glance

The family relationships are easier to hold in mind as a short comparison than as a list of separate facts.

Free CoA is the empty carrier, its thiol group unoccupied and ready to accept an acyl group. Acetyl-CoA is CoA carrying a two carbon acetyl group, and it is the central hub, feeding the citric acid cycle, fatty acid synthesis, ketogenesis, cholesterol synthesis, acetylcholine synthesis, and protein acetylation. Succinyl-CoA is CoA carrying a four carbon succinyl group and is an intermediate of the citric acid cycle itself. Malonyl-CoA is CoA carrying a three carbon malonyl group, the committed intermediate of fatty acid synthesis and a regulator that blocks fatty acid oxidation. Acyl-CoA is the general term for any loaded carrier, including the long chain fatty acyl-CoAs of beta-oxidation.

Common Confusions About Coenzyme A and Acetyl-CoA

Several misunderstandings recur in student questions, and each has a short correction.

First, CoA is not an enzyme. It is a coenzyme, a small helper molecule that enzymes use. The pyruvate dehydrogenase complex is the enzyme. CoA is one of its substrates and products.

Second, acetyl-CoA is not a fuel that is burned directly. Its acetyl group is oxidized step by step in the citric acid cycle, and the energy is captured in NADH, FADH2, and a small amount of ATP or GTP. Saying acetyl-CoA “produces energy” is shorthand for that longer process.

Third, acetyl-CoA does not cross the inner mitochondrial membrane. Citrate does, and ATP-citrate lyase regenerates acetyl-CoA on the other side. Any explanation that has acetyl-CoA itself slipping across that membrane has skipped the shuttle.

Fourth, CoA is not the same as vitamin B5. Pantothenic acid is one building block of CoA, but CoA also contains a nucleotide portion and a cysteamine arm. This article makes no claim about supplements or intake levels.

Fifth, the citric acid cycle does not consume oxygen directly. It produces NADH and FADH2, which deliver electrons to the electron transport chain, where oxygen acts as the final electron acceptor. That is why the cycle stalls without oxygen even though no step in the cycle itself uses oxygen.

Sixth, fatty acid synthesis and beta-oxidation are not the same pathway run backward. They use different enzymes, different compartments, and different carriers, and they are regulated in opposite directions.

Why Coenzyme A and Acetyl-CoA Matter Beyond the Textbook

For a student, this pair unlocks the map of metabolism. Once the carrier idea is clear, the citric acid cycle, beta-oxidation, fatty acid synthesis, ketogenesis, and cholesterol synthesis stop looking like separate lists and start looking like variations on one theme: load a carbon group onto CoA, move it, unload it, and reuse the carrier.

For a reader interested in how the body handles different fuels, acetyl-CoA explains a puzzle that otherwise looks strange. Carbohydrates, fats, and proteins are chemically very different, yet the body can switch between them for energy. The explanation is convergence: all three fuel types are broken down into acetyl-CoA or into citric acid cycle intermediates, and from that shared pool the cell can either extract energy or build new molecules.

For a reader interested in regulation, the pair shows how metabolism senses itself. The ratio of acetyl-CoA to free CoA, the level of ATP, the level of NADH, and the level of malonyl-CoA all feed back on the enzymes that make and consume acetyl-CoA. Metabolism is not a set of pipes with fixed flow rates. It is a network that adjusts its own valves based on what it measures, and acetyl-CoA is one of the main measurements.

Frequently Asked Questions

What is the difference between coenzyme A and acetyl-CoA?

Coenzyme A is the empty carrier molecule. Acetyl-CoA is that same carrier with a two carbon acetyl group attached to its thiol group through a thioester bond. Free CoA accepts acetyl groups, acetyl-CoA delivers them, and after delivery CoA is free again.

What is coenzyme A made of?

CoA is built from pantothenic acid (vitamin B5), a nucleotide portion related to adenosine diphosphate with a 3 prime phosphate, and a cysteamine arm ending in a thiol group. The thiol group is where acyl groups attach.

How is acetyl-CoA formed?

The main routes are conversion of pyruvate by the pyruvate dehydrogenase complex in mitochondria, beta-oxidation of fatty acids, breakdown of certain amino acids, and direct joining of acetate to CoA by acetyl-CoA synthetase. Which route dominates depends on the fuel available and the tissue.

Where in the cell is acetyl-CoA made?

Mitochondrial acetyl-CoA is made in the mitochondrial matrix by the pyruvate dehydrogenase complex and by beta-oxidation. Cytosolic acetyl-CoA is made mainly by ATP-citrate lyase acting on exported citrate, and by acetyl-CoA synthetase acting on acetate. Nuclear acetyl-CoA is supplied by local enzymes for histone acetylation.

What does acetyl-CoA do in the citric acid cycle?

It delivers its two carbon acetyl group to oxaloacetate to form citrate, the first step of the cycle. CoA is released in that step and reused. Each turn of the cycle then releases two carbon dioxide molecules and produces three NADH, one FADH2, and one ATP or GTP.

Can acetyl-CoA cross the mitochondrial membrane?

No. Acetyl-CoA itself cannot cross the inner mitochondrial membrane. Its carbon reaches the cytosol as citrate, which is exported and then split by ATP-citrate lyase back into acetyl-CoA and oxaloacetate. This is called the citrate shuttle.

Is acetyl-CoA used to make fat?

Yes. Cytosolic acetyl-CoA is converted by acetyl-CoA carboxylase to malonyl-CoA, the first committed step of fatty acid synthesis. The fatty acid synthase complex then builds palmitate, a 16 carbon fatty acid, by repeated addition of two carbon units.

Is acetyl-CoA the same as acetate?

No. Acetate is a two carbon acid, essentially the acetyl group with a hydroxyl group instead of a CoA attachment. Acetyl-CoA is the activated form, with the acetyl group bound to CoA through a thioester bond, which makes it reactive enough for enzymes to use.

Why is acetyl-CoA called a central metabolite?

Because it sits at the junction of carbohydrate, fat, and protein metabolism. Fuels converge on acetyl-CoA for energy extraction, and biosynthetic pathways diverge from it to make fatty acids, cholesterol, ketone bodies, acetylcholine, and acetylated proteins.

Sources & references

• OpenStax, Biology 2e, Section 7.3: Oxidation of Pyruvate and the Citric Acid Cycle. Pyruvate conversion to acetyl-CoA, CoA derived from vitamin B5, citric acid cycle steps and per turn yields, feedback regulation, and the amphibolic nature of the cycle. https://openstax.org/books/biology-2e/pages/7-3-oxidation-of-pyruvate-and-the-citric-acid-cycle
• US National Library of Medicine, StatPearls: Physiology, Krebs Cycle (NCBI Bookshelf). Acetyl-CoA defined as an acetyl group plus coenzyme A, glycolysis as the preferred source, cycle location in the mitochondrial matrix, and NADH inhibition of the cycle. https://www.ncbi.nlm.nih.gov/books/NBK556032/
• US National Library of Medicine, StatPearls: Biochemistry, Fatty Acid Oxidation (NCBI Bookshelf). Mitochondrial beta-oxidation supplying acetyl-CoA for the citric acid cycle in muscle and for ketone body synthesis in liver, and per round yields. https://www.ncbi.nlm.nih.gov/books/NBK556002/
• US National Library of Medicine, StatPearls: Biochemistry, Ketogenesis (NCBI Bookshelf). Excess acetyl-CoA directed to ketogenesis when oxaloacetate is limited, condensation to acetoacetyl-CoA, HMG-CoA formation, and acetoacetate and D-beta-hydroxybutyrate as circulating fuels. https://www.ncbi.nlm.nih.gov/books/NBK493179/
• US National Library of Medicine, PubMed Central: Coenzyme A Biochemistry review (PMC8392065). CoA as an activator of carboxylic acids, acetyl-CoA as the main CoA derivative, its roles in energy production and in fatty acid, cholesterol, bile acid, ketone body, heme, and acetylcholine synthesis, and acetyl-CoA regulation of pyruvate dehydrogenase kinase. https://pmc.ncbi.nlm.nih.gov/articles/PMC8392065/
• US National Library of Medicine, MeSH: Acetyl Coenzyme A. Acetyl-CoA participation in fatty acid and sterol biosynthesis, fatty acid oxidation, amino acid metabolism, and its role as a biological acetylating agent. https://www.ncbi.nlm.nih.gov/mesh?term="Acetyl Coenzyme A"
• ScienceDirect Topics: Acetyl-CoA Carboxylase. Acetyl-CoA carboxylase catalyzing the first committed step of fatty acid synthesis, conversion of acetyl-CoA to malonyl-CoA, ATP and bicarbonate dependence, and the biotin prosthetic group. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/acetyl-coa-carboxylase
• American Oil Chemists' Society: Plant Fatty Acid Synthesis. Acetyl-CoA carboxylase as the first committed step in fatty acid biosynthesis and the two partial reactions of the carboxylation. https://www.aocs.org/resource/plant-fatty-acid-synthesis/
• US National Library of Medicine, PubMed Central: Metabolic and Cellular Compartments of Acetyl-CoA in the Healthy and Diseased Brain (PMC9456256). Compartmentalization of acetyl-CoA, cytoplasmic acetyl-CoA correlation with acetylcholine synthesis, and nuclear acetyl-CoA supply for histone lysine acetylation. https://pmc.ncbi.nlm.nih.gov/articles/PMC9456256/
• University of Utah, NetBiochem: Fatty Acids, Extrahepatic Tissues. Ketone bodies used exclusively by extrahepatic tissues; the activating enzyme succinyl-CoA:acetoacetate-CoA transferase is absent from liver, so the liver is a net producer of ketones. https://library.med.utah.edu/NetBiochem/FattyAcids/10_3.html