Fatty acid metabolism consists of variousmetabolic processes involving or closely related tofatty acids, a family of molecules classified within thelipidmacronutrient category. These processes can mainly be divided into (1)catabolic processes that generate energy and (2)anabolic processes where they serve as building blocks for other compounds.^[1]

In catabolism, fatty acids are metabolized to produce energy, mainly in the form ofadenosine triphosphate (ATP). When compared to other macronutrient classes (carbohydrates and protein), fatty acids yield the most ATP on an energy per gram basis, when they are completely oxidized to CO₂ and water bybeta oxidation and thecitric acid cycle.^[2] Fatty acids (mainly in the form oftriglycerides) are therefore the foremost storage form of fuel in most animals, and to a lesser extent in plants.

In anabolism, intact fatty acids are important precursors to triglycerides, phospholipids, second messengers, hormones andketone bodies. For example,phospholipids form thephospholipid bilayers out of which all the membranes of the cell are constructed from fatty acids. Phospholipids comprise the plasma membrane and other membranes that enclose all theorganelles within the cells, such as thenucleus, themitochondria,endoplasmic reticulum, and theGolgi apparatus. In another type of anabolism, fatty acids are modified to form other compounds such assecond messengers andlocal hormones. Theprostaglandins made fromarachidonic acid stored in the cell membrane are probably the best-known of these local hormones.

Fatty acids are stored astriglycerides in the fat depots ofadipose tissue. Between meals they are released as follows:

• Lipolysis, the removal of the fatty acid chains from the glycerol to which they are bound in their storage form as triglycerides (or fats), is carried out bylipases. These lipases are activated by highepinephrine andglucagon levels in the blood (ornorepinephrine secreted bysympathetic nerves in adipose tissue), caused by declining bloodglucose levels after meals, which simultaneously lowers theinsulin level in the blood.^[1]
• Once freed fromglycerol, the free fatty acids enter the blood, which transports them, attached to plasmaalbumin, throughout the body.^[4]
• Long-chain free fatty acids enter metabolizing cells (i.e. most living cells in the body exceptred blood cells andneurons in thecentral nervous system) through specifictransport proteins, such as theSLC27 family fatty acid transport protein.^[5][6] Red blood cells do not containmitochondria and are therefore incapable of metabolizing fatty acids; the tissues of the central nervous system cannot use fatty acids, despite containing mitochondria, because long-chain fatty acids (as opposed to medium-chain fatty acids^[7][8]) cannot cross theblood-brain barrier^[9] into theinterstitial fluids that bathe these cells.
• Once inside the cell,long-chain-fatty-acid—CoA ligase catalyzes the reaction between a fatty acid molecule withATP (which is broken down toAMP and inorganic pyrophosphate) to give a fatty acyl-adenylate, which then reacts with freecoenzyme A to give a fattyacyl-CoA molecule.
• In order for the acyl-CoA to enter the mitochondrion the carnitine shuttle is used:^[10][11][12]

1. Acyl-CoA is transferred to the hydroxyl group of carnitine bycarnitine palmitoyltransferase I, located on the cytosolic faces of theouter andinner mitochondrial membranes.
2. Acyl-carnitine is shuttled inside by acarnitine-acylcarnitine translocase, as a carnitine is shuttled outside.
3. Acyl-carnitine is converted back to acyl-CoA bycarnitine palmitoyltransferase II, located on the interior face of theinner mitochondrial membrane. The liberated carnitine is shuttled back to the cytosol, as an acyl-CoA is shuttled into the mitochondrial matrix.

• Beta oxidation, in the mitochondrial matrix, then cuts the long carbon chains of the fatty acids (in the form of acyl-CoA molecules) into a series of two-carbon (acetate) units, which, combined withco-enzyme A, form molecules ofacetyl CoA, which condense withoxaloacetate to formcitrate at the "beginning" of thecitric acid cycle.^[2] It is convenient to think of this reaction as marking the "starting point" of the cycle, as this is when fuel - acetyl-CoA - is added to the cycle, which will be dissipated as CO₂ and H₂O with the release of a substantial quantity of energy captured in the form ofATP, during the course of each turn of the cycle and subsequentoxidative phosphorylation.

Briefly, the steps in beta oxidation are as follows:^[2]

1. Dehydrogenation byacyl-CoA dehydrogenase, yielding 1FADH₂
2. Hydration byenoyl-CoA hydratase
3. Dehydrogenation by3-hydroxyacyl-CoA dehydrogenase, yielding 1NADH + H⁺
4. Cleavage bythiolase, yielding 1acetyl-CoA and a fatty acid that has now been shortened by 2 carbons (forming a new, shortenedacyl-CoA)

This beta oxidation reaction is repeated until the fatty acid has been completely reduced toacetyl-CoA or, in the case of fatty acids with odd numbers of carbon atoms,acetyl-CoA and 1 molecule ofpropionyl-CoA per molecule of fatty acid. Each beta oxidative cut of the acyl-CoA molecule eventually yields 5ATP molecules in oxidative phosphorylation.^[13][14]

• The acetyl-CoA produced by beta oxidation enters thecitric acid cycle in the mitochondrion by combining withoxaloacetate to formcitrate. Coupled to oxidative phosphorylation this results in the complete combustion of the acetyl-CoA to CO₂ and water. The energy released in this process is captured in the form of 1GTP and 11ATP molecules per acetyl-CoA molecule oxidized.^[2][10] This is the fate of acetyl-CoA wherever beta oxidation of fatty acids occurs, except under certain circumstances in theliver.

The propionyl-CoA is later converted intosuccinyl-CoA throughbiotin-dependantpropionyl-CoA carboxylase (PCC) andVitamin B₁₂-dependantmethylmalonyl-CoA mutase (MCM), sequentially.^[15][16] Succinyl-CoA is first converted to malate, and then to pyruvate where it is then transported to the matrix to enter the citric acid cycle.

In the liver oxaloacetate can be wholly or partially diverted into thegluconeogenic pathway during fasting, starvation, a low carbohydrate diet, prolonged strenuous exercise, and in uncontrolledtype 1 diabetes mellitus. Under these circumstances, oxaloacetate is hydrogenated tomalate, which is then removed from the mitochondria of the liver cells to be converted intoglucose in the cytoplasm of the liver cells, from where it is released into the blood.^[10] In the liver, therefore, oxaloacetate is unavailable for condensation with acetyl-CoA when significant gluconeogenesis has been stimulated by low (or absent)insulin and highglucagon concentrations in the blood. Under these conditions, acetyl-CoA is diverted to the formation ofacetoacetate andbeta-hydroxybutyrate.^[10] Acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product,acetone, are frequently, but confusingly, known asketone bodies (as they are not "bodies" at all, but water-soluble chemical substances). The ketones are released by the liver into the blood. All cells with mitochondria can take up ketones from the blood and reconvert them into acetyl-CoA, which can then be used as fuel in their citric acid cycles, as no other tissue can divert its oxaloacetate into the gluconeogenic pathway in the way that this can occur in the liver. Unlike free fatty acids, ketones can cross theblood–brain barrier and are therefore available as fuel for the cells of thecentral nervous system, acting as a substitute for glucose, on which these cells normally survive.^[10] The occurrence of high levels of ketones in the blood during starvation, a low carbohydrate diet, prolonged heavy exercise, or uncontrolled type 1 diabetes mellitus is known asketosis, and, in its extreme form, in out-of-control type 1 diabetes mellitus, asketoacidosis.

The glycerol released by lipase action isphosphorylated byglycerol kinase in the liver (the only tissue in which this reaction can occur), and the resultingglycerol 3-phosphate is oxidized todihydroxyacetone phosphate. The glycolytic enzymetriose phosphate isomerase converts this compound toglyceraldehyde 3-phosphate, which is oxidized viaglycolysis, or converted to glucose viagluconeogenesis.

Fatty acids, stored as triglycerides in an organism, are a concentratedsource of energy because they contain little oxygen and areanhydrous. The energy yield from agram of fatty acids is approximately 9kcal (37 kJ), much higher than the 4 kcal (17 kJ) for carbohydrates. Since thehydrocarbon portion of fatty acids ishydrophobic, thesemolecules can be stored in a relativelyanhydrous (water-free) environment. Carbohydrates, on the other hand, are more highly hydrated. For example, 1 g ofglycogen binds approximately 2 g ofwater, which translates to 1.33 kcal/g (4 kcal/3 g). This means that fatty acids can hold more than six times the amount of energy per unit of stored mass. Put another way, if the human body relied on carbohydrates to store energy, then a person would need to carry 31 kg (67.5lb) of hydrated glycogen to have the energy equivalent to 4.6 kg (10 lb) offat.^[10]

Hibernating animals provide a good example for utilization of fat reserves as fuel. For example, bears hibernate for about 7 months, and during this entire period, the energy is derived from degradation of fat stores. Migrating birds similarly build up large fat reserves before embarking on their intercontinental journeys.^[17]

The fat stores of young adult humans average between about 10–20 kg, but vary greatly depending on gender and individual disposition.^[18] By contrast, the human body stores only about 400 g ofglycogen, of which 300 g is locked inside the skeletal muscles and is unavailable to the body as a whole. The 100 g or so of glycogen stored in the liver is depleted within one day of starvation.^[10] Thereafter the glucose that is released into the blood by the liver for general use by the body tissues has to be synthesized fromthe glucogenic amino acids and a few othergluconeogenic substrates, which do not include fatty acids.^[1] Nonetheless, lipolysis releases glycerol which can enter the pathway of gluconeogenesis.

Fatty acids are broken down to acetyl-CoA by means of beta oxidation inside the mitochondria, whereasfatty acids are synthesized from acetyl-CoA outside the mitochondria, in the cytosol. The two pathways are distinct, not only in where they occur, but also in the reactions that occur, and the substrates that are used. The two pathways are mutually inhibitory, preventing the acetyl-CoA produced by beta-oxidation from entering the synthetic pathway via theacetyl-CoA carboxylase reaction.^[1] It can also not be converted topyruvate as thepyruvate dehydrogenase complex reaction is irreversible.^[10] Instead the acetyl-CoA produced by the beta-oxidation of fatty acids condenses withoxaloacetate, to enter thecitric acid cycle. During each turn of the cycle, two carbon atoms leave the cycle as CO₂ in the decarboxylation reactions catalyzed byisocitrate dehydrogenase andalpha-ketoglutarate dehydrogenase. Thus each turn of the citric acid cycle oxidizes an acetyl-CoA unit while regenerating the oxaloacetate molecule with which the acetyl-CoA had originally combined to form citric acid. The decarboxylation reactions occur beforemalate is formed in the cycle.^[1] Only plants possess the enzymes to convert acetyl-CoA into oxaloacetate from which malate can be formed to ultimately be converted to glucose.^[1]

However, acetyl-CoA can be converted to acetoacetate, which can decarboxylate toacetone (either spontaneously, or catalyzed byacetoacetate decarboxylase). It can then be further metabolized to isopropanol which is excreted in breath/urine, or byCYP2E1 intohydroxyacetone (acetol). Acetol can be converted topropylene glycol. This converts topyruvate (by two alternative enzymes), orpropionaldehyde, or toL-lactaldehyde thenL-lactate (the common lactate isomer).^[19][20][21] Another pathway turns acetol tomethylglyoxal, then topyruvate, or toD-lactaldehyde (viaS-D-lactoyl-glutathione or otherwise) thenD-lactate.^[20][22][23] D-lactate metabolism (to glucose) is slow or impaired in humans, so most of the D-lactate is excreted in the urine; thusD-lactate derived from acetone can contribute significantly to the metabolic acidosis associated with ketosis or isopropanol intoxication.^[20]L-Lactate can complete the net conversion of fatty acids into glucose. The first experiment to show conversion of acetone to glucose was carried out in 1951. This, and further experiments used carbonisotopic labelling.^[21] Up to 11% of the glucose can be derived from acetone during starvation in humans.^[21]

The glycerol released into the blood during thelipolysis of triglycerides in adipose tissue can only be taken up by the liver. Here it is converted intoglycerol 3-phosphate by the action ofglycerol kinase which hydrolyzes one molecule ofATP per glycerol molecule which is phosphorylated. Glycerol 3-phosphate is then oxidized todihydroxyacetone phosphate, which is, in turn, converted intoglyceraldehyde 3-phosphate by the enzymetriose phosphate isomerase. From here the three carbon atoms of the original glycerol can be oxidized viaglycolysis, or converted to glucose viagluconeogenesis.^[10]

Fatty acids are an integral part of the phospholipids that make up the bulk of theplasma membranes, or cell membranes, of cells. These phospholipids can be cleaved intodiacylglycerol (DAG) andinositol trisphosphate (IP₃) throughhydrolysis of the phospholipid,phosphatidylinositol 4,5-bisphosphate (PIP₂), by the cell membrane bound enzymephospholipase C (PLC).^[24]

One product of fatty acid metabolism are theprostaglandins, compounds having diversehormone-like effects in animals. Prostaglandins have been found in almost everytissue in humans and other animals. They areenzymatically derived from arachidonic acid, a 20-carbon polyunsaturated fatty acid. Every prostaglandin therefore contains 20carbon atoms, including a5-carbon ring. They are a subclass ofeicosanoids and form theprostanoid class of fatty acid derivatives.^[25]

The prostaglandins are synthesized in the cell membrane by the cleavage of arachidonate from the phospholipids that make up the membrane. This is catalyzed either byphospholipase A₂ acting directly on a membrane phospholipid, or by a lipase acting on DAG (diacyl-glycerol). The arachidonate is then acted upon by thecyclooxygenase component ofprostaglandin synthase. This forms acyclopentane ring roughly in the middle of the fatty acid chain. The reaction also adds 4 oxygen atoms derived from two molecules of O₂. The resulting molecule is prostaglandin G₂, which is converted by the hydroperoxidase component of the enzyme complex into prostaglandin H₂. This highly unstable compound is rapidly transformed into other prostaglandins, prostacyclin and thromboxanes.^[25] These are then released into the interstitial fluids surrounding the cells that have manufactured the eicosanoid hormone.

If arachidonate is acted upon by alipoxygenase instead of cyclooxygenase,hydroxyeicosatetraenoic acids andleukotrienes are formed. They also act as local hormones.

Prostaglandins have two derivatives:prostacyclins andthromboxanes. Prostacyclins are powerful locally actingvasodilators and inhibit the aggregation of bloodplatelets. Through their role in vasodilation, prostacyclins are also involved ininflammation. They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the contraction ofsmooth muscle tissue.^[26] Conversely, thromboxanes (produced by platelet cells) arevasoconstrictors and facilitate platelet aggregation. Their name comes from their role in clot formation (thrombosis).

A significant proportion of the fatty acids in the body are obtained from the diet, in the form of triglycerides of either animal or plant origin. The fatty acids in the fats obtained from land animals tend to be saturated, whereas the fatty acids in the triglycerides of fish and plants are often polyunsaturated and therefore present as oils.

Thesetriglycerides cannot be absorbed by theintestine.^[27] They are broken down intomono- anddi-glycerides plus free fatty acids (but no free glycerol) bypancreatic lipase, which forms a 1:1 complex with a protein calledcolipase (also a constituent of pancreatic juice), which is necessary for its activity. Theactivated complex can work only at a water-fat interface. Therefore, it is essential that fats are firstemulsified bybile salts for optimal activity of these enzymes.^[28] The digestion products consisting of a mixture of tri-, di- and monoglycerides and free fatty acids, which, together with the other fat soluble contents of the diet (e.g. the fat soluble vitamins and cholesterol) and bile salts form mixedmicelles, in the watery duodenal contents (see diagrams on the right).^[27][29]

The contents of these micelles (but not the bile salts) enter theenterocytes (epithelial cells lining the small intestine) where they are resynthesized into triglycerides, and packaged intochylomicrons which are released into thelacteals (the capillaries of thelymph system of the intestines).^[30] These lacteals drain into thethoracic duct which empties into the venous blood at the junction of the left jugular and left subclavian veins on the lower left hand side of the neck. This means that the fat-soluble products of digestion are discharged directly into the general circulation, without first passing through the liver, unlike all other digestion products. The reason for this peculiarity is unknown.^[31]

The chylomicrons circulate throughout the body, giving theblood plasma a milky or creamy appearance after a fatty meal.^{[citation needed]}Lipoprotein lipase on theendothelial surfaces of the capillaries, especially inadipose tissue, but to a lesser extent also in other tissues, partially digests the chylomicrons into free fatty acids, glycerol and chylomicron remnants. The fatty acids are absorbed by the adipocytes^{[citation needed]}, but the glycerol andchylomicron remnants remain in the blood plasma, ultimately to be removed from the circulation by the liver. The free fatty acids released by the digestion of the chylomicrons are absorbed by the adipocytes^{[citation needed]}, where they are resynthesized into triglycerides using glycerol derived from glucose in theglycolytic pathway^{[citation needed]}. These triglycerides are stored, until needed for the fuel requirements of other tissues, in the fat droplet of theadipocyte.

Theliver absorbs a proportion of the glucose from the blood in theportal vein coming from the intestines. After the liver has replenished itsglycogen stores (which amount to only about 100 g of glycogen when full) much of the rest of the glucose is converted into fatty acids as described below. These fatty acids are combined with glycerol to form triglycerides which are packaged into droplets very similar to chylomicrons, but known asvery low-density lipoproteins (VLDL). These VLDL droplets are processed in exactly the same manner as chylomicrons, except that the VLDL remnant is known as anintermediate-density lipoprotein (IDL), which is capable of scavenging cholesterol from the blood. This converts IDL intolow-density lipoprotein (LDL), which is taken up by cells that require cholesterol for incorporation into their cell membranes or for synthetic purposes (e.g. the formation of thesteroid hormones). The remainder of the LDLs is removed by the liver.^[32]

Adipose tissue and lactatingmammary glands also take up glucose from the blood for conversion into triglycerides. This occurs in the same way as in the liver, except that these tissues do not release the triglycerides thus produced as VLDL into the blood. Adipose tissue cells store the triglycerides in their fat droplets, ultimately to release them again as free fatty acids and glycerol into the blood (as describedabove), when the plasma concentration of insulin is low, and that of glucagon and/or epinephrine is high.^[33] Mammary glands discharge the fat (as cream fat droplets) into the milk that they produce under the influence of theanterior pituitary hormoneprolactin.

All cells in the body need to manufacture and maintain their membranes and the membranes of their organelles. Whether they rely entirely on free fatty acids absorbed from the blood, or are able to synthesize their own fatty acids from blood glucose, is not known. The cells of thecentral nervous system will almost certainly have the capability of manufacturing their own fatty acids, as these molecules cannot reach them through theblood–brain barrier.^[34] However, it is unknown how they are reached by theessential fatty acids, which mammals cannot synthesize themselves but are nevertheless important components of cell membranes (andother functions described above).

Much likebeta-oxidation, straight-chain fatty acid synthesis occurs via the six recurring reactions shown below, until the 16-carbonpalmitic acid is produced.^[35][36]

The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found inEscherichia coli.^[35] These reactions are performed byfatty acid synthase II (FASII), which in general contains multiple enzymes that act as one complex. FASII is present inprokaryotes, plants, fungi, and parasites, as well as inmitochondria.^[37]

In animals as well as some fungi such as yeast, these same reactions occur on fatty acid synthase I (FASI), a large dimeric protein that has all of the enzymatic activities required to create a fatty acid. FASI is less efficient than FASII; however, it allows for the formation of more molecules, including "medium-chain" fatty acids via early chain termination.^[37] Enzymes, acyltransferases and transacylases, incorporate fatty acids in phospholipids, triacylglycerols, etc. by transferring fatty acids between an acyl acceptor and donor. They also have the task of synthesizing bioactive lipids as well as their precursor molecules.^[38]

Once a 16:0 carbon fatty acid has been formed, it can undergo a number of modifications, resulting in desaturation and/or elongation. Elongation, starting with stearate (18:0), is performed mainly in theendoplasmic reticulum by several membrane-bound enzymes. The enzymatic steps involved in the elongation process are principally the same as those carried out byfatty acid synthesis, but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.^[39][40]

Step	Enzyme	Reaction	Description
(a)	Acetyl-CoA:ACP transacylase		Activates acetyl-CoA for reaction with malonyl-ACP
(b)	Malonyl-CoA:ACP transacylase		Activates malonyl-CoA for reaction with acetyl-ACP
(c)	3-ketoacyl-ACP synthase		Reacts ACP-bound acyl chain with chain-extending malonyl-ACP
(d)	3-ketoacyl-ACP reductase		Reduces the carbon 3 ketone to a hydroxyl group
(e)	3-Hydroxyacyl ACP dehydrase		Eliminates water
(f)	Enoyl-ACP reductase		Reduces the C2-C3 double bond.

Abbreviations: ACP –Acyl carrier protein, CoA –Coenzyme A, NADP –Nicotinamide adenine dinucleotide phosphate.

Note that during fatty synthesis the reducing agent isNADPH, whereasNAD is the oxidizing agent inbeta-oxidation (the breakdown of fatty acids to acetyl-CoA). This difference exemplifies a general principle that NADPH is consumed during biosynthetic reactions, whereas NADH is generated in energy-yielding reactions.^[34] (Thus NADPH is also required for the synthesis ofcholesterol from acetyl-CoA; while NADH is generated duringglycolysis.) The source of the NADPH is two-fold. Whenmalate is oxidatively decarboxylated by “NADP⁺-linked malic enzyme"pyruvate, CO₂ and NADPH are formed. NADPH is also formed by thepentose phosphate pathway which converts glucose into ribose, which can be used in synthesis ofnucleotides andnucleic acids, or it can be catabolized to pyruvate.^[34]

In humans, fatty acids are formed from carbohydrates predominantly in the liver andadipose tissue, as well as in themammary glands during lactation. Thepyruvate produced byglycolysis is an important intermediary in the conversion of carbohydrates into fatty acids and cholesterol.^[34] This occurs via the conversion of pyruvate into acetyl-CoA in the mitochondrion. However, this acetyl-CoA needs to be transported into cytosol where the synthesis of fatty acids and cholesterol occurs. This cannot occur directly. To obtain cytosolic acetyl-CoA,citrate (produced by the condensation of acetyl-CoA with oxaloacetate) is removed from thecitric acid cycle and carried across the inner mitochondrial membrane into the cytosol.^[34] There it is cleaved byATP citrate lyase into acetyl-CoA and oxaloacetate. The oxaloacetate is returned to mitochondrion as malate (and then converted back into oxaloacetate to transfer more acetyl-CoA out of the mitochondrion).^[41] The cytosolic acetyl-CoA is carboxylated byacetyl-CoA carboxylase intomalonyl-CoA, the first committed step in the synthesis of fatty acids.^[41][42]

Acetyl-CoA is formed intomalonyl-CoA byacetyl-CoA carboxylase, at which point malonyl-CoA is destined to feed into the fatty acid synthesis pathway. Acetyl-CoA carboxylase is the point of regulation in saturated straight-chain fatty acid synthesis, and is subject to bothphosphorylation andallosteric regulation. Regulation by phosphorylation occurs mostly in mammals, while allosteric regulation occurs in most organisms. Allosteric control occurs as feedback inhibition by palmitoyl-CoA and activation by citrate. When there are high levels of palmitoyl-CoA, the final product of saturated fatty acid synthesis, it allosterically inactivates acetyl-CoA carboxylase to prevent a build-up of fatty acids in cells. Citrate acts to activate acetyl-CoA carboxylase under high levels, because high levels indicate that there is enough acetyl-CoA to feed into theKrebs cycle and produce energy.^[43]

High plasma levels ofinsulin in the blood plasma (e.g. after meals) cause the dephosphorylation and activation of acetyl-CoA carboxylase, thus promoting the formation of malonyl-CoA from acetyl-CoA, and consequently the conversion of carbohydrates into fatty acids, whileepinephrine andglucagon (released into the blood during starvation and exercise) cause the phosphorylation of this enzyme, inhibitinglipogenesis in favor of fatty acid oxidation viabeta-oxidation.^[34][42]

Disorders of fatty acid metabolism can be described in terms of, for example,hypertriglyceridemia (too high level oftriglycerides), or other types ofhyperlipidemia. These may be familial or acquired.

Familial types of disorders of fatty acid metabolism are generally classified asinborn errors of lipid metabolism. These disorders may be described asfatty acid oxidation disorders or as alipid storage disorders, and are any one of severalinborn errors of metabolism that result from enzyme or transport protein defects affecting the ability of the body tooxidizefatty acids in order to produce energy within muscles, liver, and othercell types. When a fatty acid oxidation disorder affects the muscles, it is ametabolic myopathy.

Moreover, cancer cells can display irregular fatty acid metabolism with regard to bothfatty acid synthesis^[44] and mitochondrialfatty acid oxidation (FAO)^[45] that are involved in diverse aspects of tumorigenesis and cell growth.

• Metabolism
• Fatty acids
• Hepatology

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