Inbiochemistry,fatty acid synthesis is the creation offatty acids fromacetyl-CoA andNADPH through the action ofenzymes. Twode novo fatty acid syntheses can be distinguished:cytosolic fatty acid synthesis (FAS/FASI) andmitochondrial fatty acid synthesis (mtFAS/mtFASII). Most of the acetyl-CoA which is converted into fatty acids is derived fromcarbohydrates via theglycolytic pathway. The glycolytic pathway also provides theglycerol with which three fatty acids can combine (by means ofester bonds) to formtriglycerides (also known as "triacylglycerols" – to distinguish them from fatty "acids" – or simply as "fat"), the final product of thelipogenic process. When only two fatty acids combine withglycerol and the thirdalcohol group isphosphorylated with a group such asphosphatidylcholine, aphospholipid is formed. Phospholipids form the bulk of thelipid bilayers that make upcell membranes and surrounds theorganelles within the cells (such as thecell nucleus,mitochondria,endoplasmic reticulum,Golgi apparatus, etc.).
Straight-chain fatty acids occur in two types: saturated and unsaturated. The latter are produced from the former.
Straight-chain fatty acid synthesis occurs via the six recurring reactions shown below, until the 16-carbonpalmitic acid is produced.[1][2]
The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found inEscherichia coli.[1] These reactions are performed byfatty acid synthase II (FASII), which in general contain multiple enzymes that act as one complex. FASII is present inprokaryotes, plants, fungi, and parasites, and also in themitochondria ofanimals, includinghumans.[3]
In animals, as well as some fungi such as yeast,de novo fatty acid synthesis in the cytosol is carried out byfatty acid synthase I (FASI), a large dimeric protein that has all of the enzymatic activities required to create a fatty acid. FASII is less efficient than FASI; however, it allows for the formation of more molecules, including"medium-chain" fatty acids via early chain termination.[3] The mitochondrial FASII system (also referred to as mtFAS) plays essential roles in mitochondrial function, such aslipoic acid biosynthesis and regulation ofrespiratory chain activity.[4]
Once formed by FASI, the 16:0 carbon fatty acid can undergo a number of modifications, resulting in desaturation and/orelongation. Elongation to stearate (18:0) mainly occurs in the ER by several membrane-bound enzymes. The steps involved in the elongation process are principally the same as those carried out by FAS, but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.[5][6]
| 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 |  | Condenses ACP-bound acyl chain with chain-extending malonyl-ACP |
| (d) | 3-ketoacyl-ACP reductase |  | Reduces the 3 keto group to hydroxyl |
| (e) | 3-Hydroxyacyl ACP dehydrase |  | Eliminates water from hydroxyl |
| (f) | Enoyl-ACP reductase |  | Reduces the C2-C3 double bond. |
| Abbreviations: ACP –Acyl carrier protein, CoA –Coenzyme A, NADP –Nicotinamide adenine dinucleotide phosphate. | |||
In 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.[7] (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" to formpyruvate, 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.[7]
In humans, fatty acids are formed from carbohydrates predominantly in theliver andadipose tissue, as well as in themammary glands during lactation.
The pyruvate produced by glycolysis is an important intermediary in the conversion of carbohydrates into fatty acids and cholesterol.[7] 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.[7] There it is cleaved byATP citrate lyase into acetyl-CoA and oxaloacetate. The oxaloacetate can be used forgluconeogenesis (in the liver), or it can be returned into mitochondrion as malate.[8] The cytosolic acetyl-CoA is carboxylated byacetyl-CoA carboxylase intomalonyl-CoA, the first committed step in the synthesis of fatty acids.[8][9]
The main fuel stored in the bodies of animals is fat. A young adult human's fat stores average between about 15–20 kg (33–44 lb), but varies greatly depending on age, sex, and individual disposition.[10] In contrast, the human body stores only about 400 g (0.9 lb) ofglycogen, of which 300 g (0.7 lb) is locked inside the skeletal muscles and is unavailable to the body as a whole. The 100 g (0.2 lb) or so of glycogen stored in the liver is depleted within one day of starvation.[11] 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.[12]
Fatty acids are broken down to acetyl-CoA by means ofbeta oxidation inside the mitochondria, whereas fatty acids are synthesized from acetyl-CoA outside the mitochondrion, 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.[12] It can also not be converted topyruvate as thepyruvate decarboxylation reaction is irreversible.[11] Instead it 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 formcitric acid. The decarboxylation reactions occur beforemalate is formed in the cycle. Malate is the only substance that can be removed from the mitochondrion to enter thegluconeogenic pathway to form glucose or glycogen in the liver or any other tissue.[12] There can therefore be no net conversion of fatty acids into glucose.
Only plants possess the enzymes toconvert acetyl-CoA into oxaloacetate from which malate can be formed to ultimately be converted to glucose.[12]
Acetyl-CoA is formed into malonyl-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 conserve energy.[13]
High plasma levels ofinsulin in the blood plasma (e.g. after meals) cause the dephosphorylation 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.[7][9]
Many bacteria use the anaerobic pathway for synthesizing unsaturated fatty acids. This pathway does not utilize oxygen and is dependent on enzymes to insert the double bond before elongation utilizing the normal fatty acid synthesis machinery. InEscherichia coli, this pathway is well understood.
Most bacteria that undergo anaerobic desaturation contain homologues of FabA and FabB.[16] Clostridia are the main exception; they have a novel enzyme, yet to be identified, that catalyzes the formation of the cis double bond.[15]
This pathway undergoestranscriptional regulation byFadR and FabR. FadR is the more extensively studied protein and has been attributed bifunctional characteristics. It acts as an activator offabA andfabB transcription and as arepressor for the β-oxidationregulon. In contrast, FabR acts as a repressor for the transcription of fabA and fabB.[14]
Aerobic desaturation is the most widespread pathway for the synthesis of unsaturated fatty acids. It is utilized in all eukaryotes and some prokaryotes. This pathway utilizesdesaturases to synthesize unsaturated fatty acids from full-length saturated fatty acid substrates.[17] All desaturases require oxygen and ultimately consume NADH even though desaturation is an oxidative process. Desaturases are specific for the double bond they induce in the substrate. InBacillus subtilis, the desaturase, Δ5-Des, is specific for inducing a cis-double bond at the Δ5 position.[8][17]Saccharomyces cerevisiae contains one desaturase, Ole1p, which induces the cis-double bond at Δ9.[8]
In mammals the aerobic desaturation is catalyzed by a complex of three membrane-bound enzymes (NADH-cytochrome b5 reductase, cytochrome b5, and adesaturase). These enzymes allow molecular oxygen,O
2, to interact with the saturated fatty acyl-CoA chain, forming a double bond and two molecules of water,H
2O. Two electrons come from NADH +H+
and two from the single bond in the fatty acid chain.[7] These mammalian enzymes are, however, incapable of introducing double bonds at carbon atoms beyond C-9 in the fatty acid chain.[nb 1].) Hence mammals cannot synthesizelinoleate orlinolenate (which have double bonds at the C-12 (= Δ12), or the C-12 and C-15 (= Δ12 and Δ15) positions, respectively, as well as at the Δ9 position), nor the polyunsaturated, 20-carbonarachidonic acid that is derived from linoleate. These are all termedessential fatty acids, meaning that they are required by the organism, but can only be supplied via the diet. (Arachidonic acid is the precursor ofprostaglandins which fulfill a wide variety of functions aslocal hormones.)[7]
Odd-chain fatty acids (OCFAs) are those fatty acids that contain an odd number of carbon atoms. The most common OCFAs are the saturated C15 and C17 derivatives, respectivelypentadecanoic acid andheptadecanoic acid.[18] The synthesis of even-chained fatty acid synthesis is done by assemblingacetyl-CoA precursors, however,propionyl-CoA instead of acetyl-CoA is used as the primer for the biosynthesis of long-chain fatty acids with an odd number of carbon atoms.[19]
InB. subtilis, this pathway is regulated by atwo-component system: DesK and DesR. DesK is a membrane-associated kinase and DesR is a transcriptional regulator of thedes gene.[8][17] The regulation responds to temperature; when there is a drop in temperature, this gene is upregulated. Unsaturated fatty acids increase the fluidity of the membrane and stabilize it under lower temperatures. DesK is the sensor protein that, when there is a decrease in temperature, will autophosphorylate. DesK-P will transfer its phosphoryl group to DesR. Two DesR-P proteins will dimerize and bind to the DNA promoters of thedes gene and recruit RNA polymerase to begin transcription.[8][17]
Pseudomonas aeruginosa
In general, both anaerobic and aerobic unsaturated fatty acid synthesis will not occur within the same system, howeverPseudomonas aeruginosa andVibrio ABE-1 are exceptions.[20][21][22]WhileP. aeruginosa undergoes primarily anaerobic desaturation, it also undergoes two aerobic pathways. One pathway utilizes a Δ9-desaturase (DesA) that catalyzes a double bond formation in membrane lipids. Another pathway uses two proteins, DesC and DesB, together to act as a Δ9-desaturase, which inserts a double bond into a saturated fatty acid-CoA molecule. This second pathway is regulated by repressor protein DesT. DesT is also a repressor offabAB expression for anaerobic desaturation when in presence of exogenous unsaturated fatty acids. This functions to coordinate the expression of the two pathways within the organism.[21][23]
Branched chain fatty acids are usually saturated and are found in two distinct families: the iso-series and anteiso-series. It has been found thatActinomycetales contain unique branch-chain fatty acid synthesis mechanisms, including that which forms tuberculosteric acid.
The branched-chain fatty acid synthesizing system usesα-keto acids as primers. This system is distinct from the branched-chain fatty acid synthetase that utilizes short-chain acyl-CoA esters as primers.[24] α-Keto acid primers are derived from thetransamination anddecarboxylation ofvaline,leucine, andisoleucine to form 2-methylpropanyl-CoA, 3-methylbutyryl-CoA, and 2-methylbutyryl-CoA, respectively.[25] 2-Methylpropanyl-CoA primers derived from valine are elongated to produce even-numbered iso-series fatty acids such as 14-methyl-pentadecanoic (isopalmitic) acid, and 3-methylbutyryl-CoA primers from leucine may be used to form odd-numbered iso-series fatty acids such as 13-methyl-tetradecanoic acid. 2-Methylbutyryl-CoA primers from isoleucine are elongated to form anteiso-series fatty acids containing an odd number of carbon atoms such as 12-Methyl tetradecanoic acid.[26] Decarboxylation of the primer precursors occurs through thebranched-chain α-keto acid decarboxylase (BCKA) enzyme. Elongation of the fatty acid follows the same biosynthetic pathway inEscherichia coli used to produce straight-chain fatty acids where malonyl-CoA is used as a chain extender.[27] The major end products are 12–17 carbon branched-chain fatty acids and their composition tends to be uniform and characteristic for many bacterial species.[26]
BCKA decarboxylase and relative activities of α-keto acid substrates
The BCKA decarboxylase enzyme is composed of two subunits in a tetrameric structure (A2B2) and is essential for the synthesis of branched-chain fatty acids. It is responsible for the decarboxylation of α-keto acids formed by the transamination of valine, leucine, and isoleucine and produces the primers used for branched-chain fatty acid synthesis. The activity of this enzyme is much higher with branched-chain α-keto acid substrates than with straight-chain substrates, and inBacillus species its specificity is highest for the isoleucine-derived α-keto-β-methylvaleric acid, followed byα-ketoisocaproate and α-ketoisovalerate.[26][27] The enzyme's high affinity toward branched-chain α-keto acids allows it to function as the primer donating system for branched-chain fatty acid synthetase.[27]
| Substrate | BCKA activity | CO2 Produced (nmol/min mg) | Km (μM) | Vmax (nmol/min mg) |
|---|---|---|---|---|
| L-α-keto-β-methyl-valerate | 100% | 19.7 | <1 | 17.8 |
| α-Ketoisovalerate | 63% | 12.4 | <1 | 13.3 |
| α-Ketoisocaproate | 38% | 7.4 | <1 | 5.6 |
| Pyruvate | 25% | 4.9 | 51.1 | 15.2 |
Factors affecting chain length and pattern distribution
α-Keto acid primers are used to produce branched-chain fatty acids that, in general, are between 12 and 17 carbons in length. The proportions of these branched-chain fatty acids tend to be uniform and consistent among a particular bacterial species but may be altered due to changes in malonyl-CoA concentration, temperature, or heat-stable factors (HSF) present.[26] All of these factors may affect chain length, and HSFs have been demonstrated to alter the specificity of BCKA decarboxylase for a particular α-keto acid substrate, thus shifting the ratio of branched-chain fatty acids produced.[26] An increase in malonyl-CoA concentration has been shown to result in a larger proportion of C17 fatty acids produced, up until the optimal concentration (≈20μM) of malonyl-CoA is reached. Decreased temperatures also tend to shift the fatty-acid distribution slightly toward C17 fatty-acids inBacillus species.[24][26]
This system functions similarly to the branch-chain fatty acid synthesizing system, however it uses short-chain carboxylic acids as primers instead of alpha-keto acids. In general, this method is used by bacteria that do not have the ability to perform the branch-chain fatty acid system using alpha-keto primers. Typical short-chain primers include isovalerate, isobutyrate, and 2-methyl butyrate. In general, the acids needed for these primers are taken up from the environment; this is often seen in ruminal bacteria.[28]
The overall reaction is:
The difference between (straight-chain) fatty acid synthase and branch-chain fatty acid synthase is substrate specificity of the enzyme that catalyzes the reaction of acyl-CoA to acyl-ACP.[24]
Omega-alicyclic fatty acids typically contain an omega-terminal propyl or butyryl cyclic group and are some of the major membrane fatty acids found in several species of bacteria. The fatty acid synthetase used to produce omega-alicyclic fatty acids is also used to produce membrane branched-chain fatty acids. In bacteria with membranes composed mainly of omega-alicyclic fatty acids, the supply of cyclic carboxylic acid-CoA esters is much greater than that of branched-chain primers.[24] The synthesis of cyclic primers is not well understood but it has been suggested that mechanism involves the conversion of sugars toshikimic acid which is then converted to cyclohexylcarboxylic acid-CoA esters that serve as primers for omega-alicyclic fatty acid synthesis[28]
Tuberculostearic acid (D-10-Methylstearic acid) is a saturated fatty acid that is known to be produced byMycobacterium spp. and two species ofStreptomyces. It is formed from the precursor oleic acid (a monounsaturated fatty acid).[29] After oleic acid is esterified to a phospholipid,S-adenosyl-methionine donates a methyl group to the double bond of oleic acid.[30] This methylation reaction forms the intermediate 10-methylene-octadecanoyal. Successive reduction of the residue, with NADPH as a cofactor, results in 10-methylstearic acid[25]
In addition to fatty acid synthesis incytosol (FAS/FASI), there is also anotherde novo fatty acid synthesis inmitochondria (mtFAS/mtFASII) ineukaryotes. This pathway was first described in 1990 inNeurospora crassa.[4][31] Mitochondrial fatty acid synthesis is essential forcellular respiration and mitochondrialbiogenesis.[32] It is also required for respiratory growth inyeast and forembryonic survival inmammals.[33]
_pathway.svg)
The mtFAS pathway consists of at least six individually present enzymes, all encoded by separate genes.[34] This sets it apart from cytosolic fatty acid synthesis, where themultifunctional enzymefatty acid synthase (FASN) contains all enzymatic activities within a singlepolypeptide chain and is encoded by a single gene.[34] Despite this structural difference, mtFAS and FAS use the same chemistry to build fatty acids.[4]
In mtFAS, mitochondrialacyl carrier protein (ACP) serves as a solublescaffold protein in themitochondrial matrix,covalently attaching the growing fatty acyl chains.[4]Malonyl-CoA—formed bymtACC1 (a mitochondrialisoform ofacetyl-CoA carboxylase 1) fromacetyl-CoA and byacyl-CoA synthetase family member 3 (ACSF3) frommalonate—serves as the chain-extender unit.[35][36] However, the precise mitochondrial source of malonyl-CoA remains under debate.[37]
In each round of chain elongation,malonyl-CoA is first transferred to ACP bymalonyl‑CoA:ACP transacylase (MCAT) to formmalonyl-ACP, which then undergoescondensation with the growing acyl-ACP (with acetyl-ACP in the first round) catalyzed by3-oxoacyl-ACP synthase (OXSM), releasingCO2 and extending the chain by twocarbons.[34] Next, the newly extended fatty acyl chain on ACP (3-ketoacyl-ACP) undergoesreduction byestradiol-17β-dehydrogenase 8 (HSD17B8) andcarbonyl reductase 4 (CBR4),dehydration by3-hydroxyacyl-ACP dehydratase 2 (HTD2), and a final reduction bytrans-2-enoyl-CoA reductase (MECR), yielding asaturated fatty acid on ACP (acyl-ACP) once again, which is then available as the substrate for the next elongation round.[34]
These steps repeat until an eight-carbon saturated fatty acid on ACP—known asoctanoyl-ACP (C8)—is formed.[4] At that point, thismedium-chain fatty acid bound to ACP can either exit the mtFAS pathway or remain for further elongation intolong-chain fatty acids (C14-C16).[4] Since no mitochondrialthioesterase has been identified in any animal species, the final product of mtFAS remains bound to ACP rather than being released as afree fatty acid.[4]
Mitochondrial fatty acid synthesis plays a crucial role in cellularenergy metabolism by generating octanoyl‑ACP (C8), which serves as the directprecursor forlipoic acid biosynthesis.[38] Lipoic acid is an essentialcofactorcovalently attached to specificlysineresidues on target enzymes in a process calledlipoylation.[39] Thispost‑translational modification is essential for the activity of key mitochondrial enzyme complexes—namely, thepyruvate dehydrogenase complex (PDC), theα‑ketoglutarate dehydrogenase complex (OGDC), the2‑oxoadipate dehydrogenase complex (2‑OADHC), thebranched‑chain α‑ketoacid dehydrogenase complex (BCKDC), and theglycine cleavage system (GCS).[39][40]
In parallel, mtFAS and its acyl‑ACP products provide a metabolic feedback mechanism, regulating mitochondrialacetyl‑CoA consumption and thereby integrating lipid synthesis with broader metabolic control.[37]
Beyond octanoyl‑ACP, mtFAS also produces longer‑chain acyl‑ACP species such asmyristoyl‑ACP (C14) andpalmitoyl‑ACP (C16), which interact with members of theleucine‑tyrosine‑arginine motif (LYRM) protein family.[4] These LYRM proteins are vital for the correct assembly and stability of theelectron‑transport chain (ETC) complexes and foriron–sulfur (Fe–S) cluster biogenesis within mitochondria.[4]
In addition to these enzymatic and structural roles, mtFAS has also been implicated as a mediator of intracellularsignal transduction. This is supported by observations that the levels of bioactive lipids—such aslysophospholipids andsphingolipids—correlate with mtFAS activity.[41] For instance,knockdown of ACP reducesceramide levels, whereas loss of the terminal mtFAS enzyme MECR results in ceramide accumulation.[41][42]
Importantly, mtFAS function extends to the regulation ofimmune cell metabolism.CRISPR/Cas9 screens have identified mtFAS genes—especiallyMecr,Mcat, andOxsm—as key regulators ofT cell metabolism.[43] While MECR is not required fornaive T cell maintenance, its loss inactivated T cells impairsproliferation,survival, anddifferentiation.[43] MECR deficiency disruptsmitochondrial respiration, altersTCA cycle activity, and increasesferroptosis sensitivity, ultimately reducing T cell fitness andinflammatory capacity.[43]
Disorders in mtFAS pathway lead to the followingmetabolic diseases:
In the following, similarities and differences between cytosolic and mitochondrial fatty acid synthesis are shown:
| Feature | Cytosolic fatty acid synthesis (FAS/FASI) | Mitochondrial fatty acid synthesis (mtFAS/mtFASII) | |
|---|---|---|---|
| Place of synthesis | Cytosol | Mitochondrial matrix[4] | |
| Enzyme system | FAS type I (multifunctional enzyme) | FAS type II (single enzymes)[4] | |
| Regulation | Key enzyme | Acetyl-CoA carboxylase | Unknown |
| Activation | Allosteric:citrate | Unknown | |
| Inhibition | Allosteric:palmitoyl-CoA | Unknown | |
| Primer | Acetyl-CoA (from mitochondria viacitrate–malate shuttle) | Acetyl-CoA (directly present in the matrix) | |
| Extender units | Malonyl-CoA (fromcarboxylation of acetyl-CoA) | Malonyl-CoA (mainly from thecarboxylation of acetyl-CoA, but also from thethioesterification ofmalonic acid) | |
| Cofactors | Reducing agent | NADPH | NADPH |
| Other | ATP,biotin (both for conversion tomalonyl-CoA) | ATP,biotin (both also formalonyl-CoA) | |
| Thioesterase | Available in cytosol | None known in mitochondria[4] | |
| Endproduct(s) | Mainlypalmitate (C16:0) | Octanoyl-ACP (C8),myristoyl-ACP (C14),palmitoyl-ACP (C16)[4] | |
| Function | Lipid storage, energy balance, membrane structure | Precursors for cofactors such aslipoic acid (forPDH complex,αKGDH complex,2-oxoadipate dehydrogenase complex,BCKDH complex andglycine cleavage system);[4][38] assembly of theelectron transport chain (ETC);[4]iron-sulfur (FeS) cluster biogenesis;[4] role inceramide metabolism[4] | |
| Participation inlipid synthesis | Central role inde novolipogenesis | Supplementary role only | |
| Phylogenetic similarity | Eukaryote-specific | Bacteria-like (evolutionary conserved)[4] | |
The positions of the double bonds in a fatty acid chain can, therefore, be indicated in two ways, using the C-n or the ω-n notation. Thus, in an 18 carbon fatty acid, a double bond between C-12 (or ω-7) and C-13 (or ω-6) is reported either as Δ12 if counted from the –COOH end (indicating only the "beginning" of the double bond), or as ω-6 (or omega-6) if counting from the-CH
3 end. The "Δ" is the Greek letter "delta", which translates into "D" (forDouble bond) in the Roman alphabet. Omega (ω) is the last letter in the Greek alphabet, and is therefore used to indicate the "last" carbon atom in the fatty acid chain. Since the ω-n notation is used almost exclusively to indicate the positions of the double bonds close to the-CH
3 end inessential fatty acids, there is no necessity for an equivalent "Δ"-like notation – the use of the "ω-n" notation always refers to the position of a double bond.
Metabolism map | ||
|---|---|---|
 Majormetabolic pathways inmetro-style map. Click any text (name of pathway or metabolites) to link to the corresponding article. Single lines: pathways common to most lifeforms. Double lines: pathways not in humans (occurs in e.g. plants, fungi, prokaryotes).  Orange nodes:carbohydrate metabolism. Violet nodes:photosynthesis. Red nodes:cellular respiration. Pink nodes:cell signaling. Blue nodes:amino acid metabolism. Grey nodes:vitamin andcofactor metabolism. Brown nodes:nucleotide andprotein metabolism. Green nodes:lipid metabolism. | ||
