1-9 A-D E-G H-M N-P Q-S T-Z


CAS number 57-10-3
PubChem CID: 985


Acid, Hexadecanoic; Acid, Palmitic; Calcium Palmitate; Hexadecanoic Acid; Palmitate, Calcium; Palmitate, Sodium; Palmitic Acid; Sodium Palmitate; palmitic acid; Hexadecanoic acid; 57-10-3; Cetylic acid; palmitate; n-Hexadecanoic acid; Hexadecylic acid; Hydrofol; n-Hexadecoic acid; 1-Pentadecanecarboxylic acid; Palmitinic acid; Pentadecanecarboxylic acid; C16 fatty acid; hexaectylic acid; Industrene 4516; Emersol 140; Emersol 143; Hystrene 8016; Hystrene 9016; 1- Hexyldecanoic Acid; hexadecoic acid; Palmitinsaeure; Palmitic acid, pure; Palmitic acid 95%; Palmitic acid (natural); Prifac 2960; FEMA No. 2832; Pristerene 4934; Edenor C16; Kortacid 1698; Lunac P 95KC; C16:0; Loxiol EP 278; Lunac P 95; Lunac P 98; Hydrofol Acid 1690; palmic acid; HSDB 5001; Fatty acids, C14-18; AI3-01594; C16H32O2; NSC 5030; UNII-2V16EO95H1; CCRIS 5443; Palmitic acid (NF); Glycon P-45; CHEBI:15756; Calcium palmitate; NSC5030; EINECS 200-312-9; Hexadecanoic acid (9CI); BRN 0607489; Palmitic acid (7CI,8CI); CHEMBL82293; CH3-[CH2]14-COOH; IPCSVZSSVZVIGE-UHFFFAOYSA-N; 2V16EO95H1;; n-hexadecoate; LMFA01010001; PA 900; FA 1695; 1-hexyldecanoate; NCGC00164358-01; DSSTox_CID_1602; pentadecanecarboxylate; DSSTox_RID_76229; DSSTox_GSID_21602; FAT; PLM; Hexadecanoate (n-C16:0); CAS-57-10-3; SR-01000944716; Palmitic acid [USAN:NF];; palmitoatei; Hexadecoate; Palmitinate; palmitic-acid; palmitoic acid; Aethalic acid; Hexadecanoic acid Palmitic acid; (C14-C18)Alkylcarboxylic acid; 2hmb; 2hnx; (C14-C18) Alkylcarboxylic acid; Fatty acid pathway; Palmitic acid_jeyam; EINECS 266-926-4; Kortacid 1695; Palmitic acid_RaGuSa; Univol U332; Prifrac 2960; Hexadecanoic acid anion; 3v2q; ACMC-1ASQF; SDA 17-005-00i Palmitic acid, >=99%; bmse000590; D0KS1O; Epitope ID:141181; C16:0 (Lipid numbers); EC 200-312-9; AC1L1AH2; SCHEMBL6177; 4-02-00-01157 (Beilstein Handbook Reference); KSC270O2R; WLN: QV15; P5585_SIGMA; GTPL1055; QSPL 166; Palmitic acid, 95% 500g; DTXSID2021602; CTK1H0728; hexadecanoic acid (palmitic acid); 1b56; MolPort-001-780-241; HMS3649N08; Palmitic acid, analytical standard; Palmitic acid, BioXtra, >=99%; Palmitic acid, Grade II, ~95%; BB_SC-09400; NSC-5030; Palmitic acid, natural, 98%, FG; ZINC6072466; Tox21_112105; Tox21_201671; Tox21_302966; ANW-13574; BBL011563; BDBM50152850; SBB017229; STL146733; Palmitic acid, >=95%, FCC, FG; AKOS005720983; Light end (C14-C18) saturated fatty acid fraction from tallow fatty acids; Tox21_112105_1; DB03796; FA 16:0; LS-2331; MCULE-1361949901; Palmitic acid, for synthesis, 98.0%; RP29137; RTC-060456; SEL10404124; NCGC00164358-02; NCGC00164358-03; NCGC00256424-01; NCGC00259220-01; AN-23574; I728; Palmitic acid, purum, >=98.0% (GC); SC-81752; ST023798; AB1002597; TC-060456; CS-0009861; FT-0626965; N2456; P0002; P1145; Palmitic acid, SAJ first grade, >=95.0%; ST24025707; C00249; D05341; Palmitic acid, Vetec(TM) reagent grade, 98%; Palmitic acid, >=98% palmitic acid basis (GC); S04-0102; SR-01000944716-1; SR-01000944716-2; BA71C79B-C9B1-451A-A5BE-B480B5CC7D0C; F0001-1488;; Z955123552; Palmitic acid, certified reference; material, TraceCERT(R); UNII-13FB83DEYU component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-44NH37HHP9 component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-5U9XZ261ER component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-7N137Q0QYJ component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-96GS7P39SN component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-B6G0Y5Z616 component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-D1CZ545P7Z component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-HBA528N3PW component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-MO7HV04S9Y component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-ODL221H4AM component IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-Q8Y7S3B85M component; IPCSVZSSVZVIGE-UHFFFAOYSA-N; UNII-V1PY73ZXPE component IPCSVZSSVZVIGE-UHFFFAOYSA-N; Palmitic acid, European Pharmacopoeia (EP) Reference Standard; UNII-79P21R4317 component IPCSVZSSVZVIGE-UHFFFAOYSA-N; Palmitic acid, United States Pharmacopeia (USP) Reference Standard; Palmitic acid, Pharmaceutical Secondary Standard; Certified Reference Material; 116860-99-2; 212625-86-0; 60605-23-4; 66321-94-6; 8045-38-3; Sodium Palmitate, Palmitic acid sodium salt, Sodium hexadecanoate, Sodium pentadecanecarboxylate, HSDB 759; palimitik asit; palimtik asit; palimitik asid; palimtik asid; palmıtıc asid; palmıtıc asit



Technical Information
Formal Name : hexadecanoic acid
Molecular Formula: C16H32O2
Formula Weight: 256.4
Purity ≥98%
Formulation: A crystalline solid
InChi Code : InChI=1S/C16H32O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16(17)18/h2-15H2,1H3,(H,17,18)
Origin : Plant/Palm
Side Chain Carbon Sum 16:0
Shipping & Storage Information
Storage -20°C
Shipping : Room Temperature in continental US; may vary elsewhere
Stability ≥ 2 years
Palmitic Acid: Physiological Role, Metabolism and Nutritional ImplicationsAbstract
Palmitic acid (PA) has been for long time negatively depicted for its putative detrimental health effects, shadowing its multiple crucial physiological activities. PA is the most common saturated fatty acid accounting for 20-30% of total fatty acids in the human body and can be provided in the diet or synthesized endogenously via de novo lipogenesis (DNL). PA tissue content seems to be controlled around a well-defined concentration, and changes in its intake do not influence significantly its tissue concentration because the exogenous source is counterbalanced by PA endogenous biosynthesis. Particular physiopathological conditions and nutritional factors may strongly induce DNL, resulting in increased tissue content of PA and disrupted homeostatic control of its tissue concentration. The tight homeostatic control of PA tissue concentration is likely related to its fundamental physiological role to guarantee membrane physical properties but also to consent protein palmitoylation, palmitoylethanolamide (PEA) biosynthesis, and in the lung an efficient surfactant activity. In order to maintain membrane phospholipids (PL) balance may be crucial an optimal intake of PA in a certain ratio with unsaturated fatty acids, especially PUFAs of both n-6 and n-3 families. However, in presence of other factors such as positive energy balance, excessive intake of carbohydrates (in particular mono and disaccharides), and a sedentary lifestyle, the mechanisms to maintain a steady state of PA concentration may be disrupted leading to an over accumulation of tissue PA resulting in dyslipidemia, hyperglycemia, increased ectopic fat accumulation and increased inflammatory tone via toll-like receptor 4. It is therefore likely that the controversial data on the association of dietary PA with detrimental health effects, may be related to an excessive imbalance of dietary PA/PUFA ratio which, in certain physiopathological conditions, and in presence of an enhanced DNL, may further accelerate these deleterious effects.Introduction
Palmitic acid (16:0, PA) is the most common saturated fatty acid found in the human body and can be provided in the diet or synthesized endogenously from other fatty acids, carbohydrates and amino acids. PA represents 20-30% of total fatty acids (FA) in membrane phospholipids (PL), and adipose triacylglycerols (TAG) (Carta et al., 2015). On average, a 70-kg man is made up of 3.5 Kg of PA. As the name suggests, PA is a major component of palm oil (44% of total fats), but significant amounts of PA can also be found in meat and dairy products (50-60% of total fats), as well as cocoa butter (26%) and olive oil (8-20%). Furthermore, PA is present in breast milk with 20-30% of total fats (Innis, 2016). The average intake of PA is around 20-30 g/d representing about 8-10 en% (Sette et al., 2011). PA tissue content seems to be controlled around a well-defined concentration, since changes in its intake do not influence significantly its tissue concentration (Innis and Dyer, 1997; Song et al., 2017), because the intake is counterbalanced by PA endogenous biosynthesis via de novo lipogenesis (DNL). Particular physiopathological conditions and nutritional factors may strongly induce DNL, resulting in increased tissue content of PA and disrupted homeostatic control of its tissue concentration (Wilke et al., 2009). However, under normal physiological conditions, PA accumulation is prevented by enhanced delta 9 desaturation to palmitoleic acid (16:1n-7, POA) and/or elongation to stearic acid (SA) and further delta 9 desaturation to oleic acid (18:1, OA) (Strable and Ntambi, 2010; Silbernagel et al., 2012). The tight homeostatic control of PA tissue concentration is likely related to its fundamental physiological role in several biological functions. Particularly in infants PA seems to play a crucial role as recently thoroughly revised by Innis (Innis, 2016). The disruption of PA homeostatic balance, implicated in different physiopathological conditions such as atherosclerosis, neurodegenerative diseases and cancer, is often related to an uncontrolled PA endogenous biosynthesis, irrespective of its dietary contribution.Endogenous PA biosynthesis by DNL and metabolic outcomes
FA synthesis starts with citrate conversion to acetyl-CoA and then malonyl-CoA, which is then elongated to form palmitate and other FA. Key enzymes in this process are acetyl-CoA carboxylase (ACC), which catalyzes the DNL limiting step reaction, and the FA synthase (FAS). The main sources of citrate for DNL are glucose and glutamine-derived α-ketoglutarate (α-KG), especially under hypoxia or disruption of the mitochondrial oxidative machinery (Vernieri et al., 2016). Carbohydrate feeding, beyond the body capacity to store it as glycogen or use it as energy substrate, promotes DNL by inducing a raise of insulin and substrate availability (Cohen et al., 2011). Insulin stimulates the transcription factor Sterol Regulatory Element-Binding Proteins-1c (SREBP-1c) which up-regulates the enzymes that catalyze lipogenesis (Horton et al., 2002). Glucose also stimulates lipogenesis by activating the transcription factor of carbohydrate-binding protein (ChREBP) (Uyeda and Repa, 2006). Like SREBP-1c, ChREBP induces different genes involved in fatty acid biosynthesis (Uyeda and Repa, 2006). Unlike glucose, fructose, being taken up almost totally by the liver (Tappy and Le, 2010), cannot be used for glycogen biosynthesis and is promptly converted to glyceraldehyde-3-phosphate, providing a substrate for DNL. The yearly consumption of fructose has gradually increased and likely contributes to the raise of non-alcoholic fatty liver disease (NAFLD) (Cohen et al., 2011).
DNL is a highly conserved pathway also present in invertebrate species where the survival capability seems to be related to their ability to store energy reserves as fat from different sugars in the diet (Biolchini et al., 2017).
In humans, in post-prandial state, dietary carbohydrates could provide a potential source of liver FA through the DNL process (Donnelly et al., 2005). Most of the studies conducted on fasting subjects showed however that the contribution of DNL to the total pool of hepatic FA was modest in healthy subjects in a regular diet. Whereas, conditions such as obesity, insulin resistance as well as NAFLD, DNL has been found markedly induced, heavily contributing to liver fat deposition and changes in fatty acid composition (Marques-Lopes et al., 2001). Moreover, differences in DNL rates found in different studies were related to fasted or post-prandial state, since DNL is suppressed by fasting (Schwarz et al., 1995). Another confounding factor is the role of fatty acids binding proteins (FABP), indeed Cao et al. (2008), found that FABP greatly determined the impact of dietary fat on adipose lipid composition and metabolism. In fact, in the absence of these fatty acid chaperones, adipose tissue markedly relies on DNL.
From fasting studies in patients with NAFLD, excessive uptake of FA in the liver could be attributed to insulin resistance in adipose tissue (Fabbrini et al., 2008). Lambert and colleagues observed that in patients with non-alcoholic fatty liver (NAFL) DNL rates were correlated to the amount of liver fat deposition. Triacylglycerol PA, from DNL, was also increased, and the values were independently associated to intrahepatic TAG (Lambert et al., 2014).
When DNL is increased by short-term supply of high carbohydrate foods in humans, a central enzyme, stearoyl-CoA desaturase (SCD), is regulated in parallel with the DNL pathway (Chong et al., 2008; Collins et al., 2010). In human adipocytes, PA derived from DNL is preferably elongated and desaturated with respect to the exogenous PA, suggesting that DNL can serve as a key regulator in concert with elongation and desaturation to maintain cell membrane fluidity and insulin sensitivity (Collins et al., 2010), lowering PA tissue concentration.
An increase of SCD1 activity in obese subjects has been associated to lower fat oxidation and higher fat storage (Hulver et al., 2005). However, it has also been reported a link between SCD1 content and insulin sensitivity in humans (Peter et al., 2009), and a protection against fat-induced insulin resistance in rat muscle cells was observed following a transient increase of SCD1 content (Pinnamaneni et al., 2006; Bergman et al., 2010). This may suggest that desaturation of de novo synthesized FA may be required to modulate TAG biosynthesis and prevent lipotoxic effects by excessive saturated fat accumulation (Collins et al., 2010), and consequent cellular dysfunction involved in the metabolic syndrome (Brookheart et al., 2009; Cnop et al., 2012). It is still debated whether POA, the SCD1 product of PA, is one of the major responsible of such activities, as recently thoroughly reviewed (Souza et al., 2017).
Therefore, overproduction of PA by DNL, activated by physiopathological conditions and chronic nutritional imbalance, leads to a systemic inflammatory response and a metabolic dysregulation, resulting in dyslipidemia, insulin resistance and a dysregulated fat deposition and distribution (Donnelly et al., 2005). Remarkably, a recent study has shown that taste sensitivity to 6-n-propylthiouracil (PROP), a genetic trait of oral chemosensory perception, can influence DNL, and therefore PA red blood cell levels, in association to changes in circulating endocannabinoid levels (Carta et al., 2017). Noteworthy, it has been shown that treatment with endocannabinoid receptor agonist increased DNL in the mouse liver or in isolated hepatocytes (Osei-Hyiaman et al., 2005). Thus, endocannabinoids may influence DNL rate either directly and/or regulating food intake according to PROP sensitivity (Tomassini Barbarossa et al., 2013).DNL and cancer
The association of circulating PA levels with cancer development is quite controversial. Association between PA levels in blood fraction in relation to breast cancer risk has been reported in a meta-analysis (Saadatian-Elahi et al., 2004) and a prospective study (Bassett et al., 2016), whereas another prospective study conducted in northern Italy found no association between saturated fatty acids and breast cancer risk (Pala et al., 2001). Since changes in PA intake do not influence significantly its tissue concentration (Innis and Dyer, 1997; Song et al., 2017), it implies that DNL has a central role in cancerogenesis.
DNL is a distinctive pathway of most cancer cells. In fact, although most normal cells use dietary or fatty tissue-derived FA that circulate in the bloodstream either as FFA bound to albumin or as part of lipoproteins, most cancer cells de novo synthetize their FA independently from nutrient availability and hormone stimulation (Menendez and Lupu, 2007).
The enhanced DNL in cancer cells is strictly linked to the so-called Warburg effect (Vander Heiden et al., 2009). Warburg found that unlike most normal tissues, cancer cells preferentially use anaerobic glycolysis even in the presence of adequate oxygen supply which would be sufficient to support mitochondrial oxidative phosphorylation, and therefore their metabolism is frequently referred to as "aerobic glycolysis" or Warburg effect (Warburg, 1956). Apparently, Warburg effect seems not to be suitable to meet energy requirements of proliferating cells by not fully taking advantage of complete catabolism of glucose using mitochondrial oxidative phosphorylation to maximize ATP production. In addition, it was shown that it was not due to an impaired mitochondria activity, with consequent compromised aerobic respiration and a reliance on glycolytic metabolism, as first was hypothesized (Warburg, 1956), but later confuted (Weinhouse, 1976; Fantin et al., 2006; Moreno-Sanchez et al., 2007), hypothesizing a different explanation for "aerobic glycolysis" in cancer cells.
Anaerobic glycolysis generates only 2 ATPs per molecule of glucose, while oxidative phosphorylation produces up to 36 ATPs upon total oxidation of one glucose molecule. Therefore, why a metabolism that produces less ATP would be selected for in proliferating cells?
Lower ATP production might be a problem when energy substrates are limited, but not in the case of proliferating mammalian cells, continuously supplied with nutrients from blood, showing high ratios of ATP/ADP and NADH/NAD+ (Christofk et al., 2008; DeBerardinis et al., 2008). Moreover, even small decreases in the ATP/ADP ratio can impair growth, leading cells deficient in ATP to apoptosis (Vander Heiden et al., 1999; Izyumov et al., 2004).
A clarification for the peculiar energy metabolism of proliferating cells is the metabolic requirements that extend beyond ATP.
In fact, proliferating cell must replicate all its cellular contents, which requires nucleotides, amino acids, and lipids biosyntheses. Focusing on DNL, synthesis of PA needs 7 molecules of ATP, 16 carbons from 8 molecules of acetyl-CoA, and 28 electrons from 14 molecules of NADPH.
The production of a 16-carbon fatty acyl chain requires one glucose molecule that, if completely oxidized, can provide five times the ATP necessary, while to produce the required NADPH, 7 glucose molecules are needed. This high asymmetry is only moderately balanced by the consumption of 3 glucose molecules in acetyl-CoA synthesis to satisfy the carbon necessity of the acyl chain. For the cellular proliferation, the amount of the glucose cannot be committed to carbon catabolism for ATP production; indeed, this would give an increase in the ATP/ADP ratio that would severely impair the flux through glycolytic intermediates, reducing the synthesis of the acetyl-CoA and NADPH needed for macromolecular production (Vander Heiden et al., 2009).
If this were the case, the complete conversion of glucose to CO2 via oxidative phosphorylation in the mitochondria to maximize ATP production would contrast the requirements of a proliferating cell.
Changes in the correct balance of fuels and/or signal transduction pathways that concern nutrient utilization may trigger the cancer predisposition related to metabolic diseases such as diabetes and obesity (Calle and Kaaks, 2004; Pollak, 2008).
AMP-activated protein kinase (AMPK) is a dominant regulator of metabolism, and key energy sensor of intracellular AMP/ATP ratios. When there is an increase of this ratio (low energy conditions), two molecules of AMP bind, and consequently AMPK is activated (Ellingson et al., 2007). AMPK simultaneously inhibits anabolic pathways, as lipogenesis, and activates catabolic ones such as FA oxidation and glucose uptake (Winder and Hardie, 1999).
Interestingly, CD36, a scavenger receptor that modulates the uptake of long chain fatty acid (LCFA) in high affinity tissues and contributes, under excessive fat supply, to lipid accumulation and metabolic dysfunction signaling (Pepino et al., 2014), might influence AMPK activation.
Palmitic Acid
Palmitic acid (97.3%) is more readily absorbed than stearic acid (94.1%), while other fatty acids (lauric, myristic, oleic, elaidic, and linoleic acids) are nearly completely absorbed (>99.0%) (Baer et al., 2003).Palmitic Acid
Palmitic acid forms a large proportion of total dietary SFA intake and can be found in palm oil, meat, and butter. Palmitic acid can also be synthesized endogenously by elongation of C14:0, although this pathway is thought to be less active in the context of Western, high-fat diets (Hellerstein, 1999) and it is by far the largest component of circulating SFAs (Khaw et al., 2012; Wu et al., 2011). Various studies have investigated the association of circulating palmitic acid with CHD, with conflicting results. One of these is the CHS, a community-based prospective study in the United States among men and women aged 65 years and older (Wu et al., 2011). In this population, palmitic acid contributed 25.3% to the total fatty acids measured. The authors reported no association of CHD risk between subjects with levels in the top versus bottom fifth of the distribution of palmitic acid, after adjusting for a range of potential confounding risk factors (Wu et al., 2011). Similarly, no association was found in another US-based study, Atherosclerosis Risk in Communities (ARIC; Wang et al., 2003a), and in a Japanese study, Japan EPA Lipid Intervention Study (JELIS; Itakura et al., 2011). A potential detrimental effect was reported in the subjects at high baseline cardiovascular risk enrolled in multiple risk factor intervention trial (MRFIT), although only when levels of palmitic acid were measured in cholesterol esters (CEs; Simon et al., 1995). When measured in PLs, no significant association was observed. However, the minimally adjusted association of CE levels of palmitic acid with CHD, like that of PL levels, was not significant. Instead, the association of palmitic acid CEs only became significant after adjusting for various factors, including smoking, a potential strong confounder, and cholesterol levels, which may be a potential mediating factor rather than confounder. Similar adjustments were not conducted for PL levels of palmitic acid.
Although differences in adjustment levels may account for some of the difference in association between CE and PL levels in this study, mean concentrations of palmitic acid in PLs (27.86%) were more than two times higher than concentrations in CEs (11.8%) (Simon et al., 1995), which is consistent with other studies reporting on fatty acid levels measured in CEs and PLs (Wang et al., 2003a). This highlights the importance of metabolic pathways in determining fatty acid levels in different blood fractions, and this should be considered when comparing results from different studies. The EPIC-Norfolk study reported a strong detrimental association in which each SD increase in PL levels of palmitic acid was associated with a 37% higher risk of CHD (Khaw et al., 2012).
The association of CE levels of palmitic acid was also investigated in Finnish subjects enrolled in European Action on Secondary and Primary Prevention through Intervention to Reduce Events (EUROASPIRE), originally a pan-European secondary CAD prevention trial (Erkkila et al., 2003). Among patients with established CAD, the authors reported that the middle tertile of palmitic acid was significantly associated with a lower risk of fatal CHD and nonfatal MI. However, there was no significant trend across tertiles (P=0.06), and as the authors rightfully noted, results from this study among CAD patients taking cardiovascular drugs should not directly be generalized to healthy populations.Comparison of Dietary Saturated Fatty Acids
Palmitic acid (16:0) is the primary saturated fatty acid in most diets. This compound constitutes about 25% of the fatty acids of beef or pork fat, but only 6-10% of the fatty acids of sunflower, safflower, peanut, or soy oils (see Table 6.8). Dietary palmitic acid increases LDL-cholesterol (Grundy and Denke, 1990). Myristic acid (14:0) is present at high levels in butterfat and in the "tropical oils" palm oil and coconut oil. Although myristic acid elevates LDL-cholesterol, it is generally a rather minor component of the diet. Stearic acid (18:0) is also a major component of many fats and oils. It constitutes 15-20% of the fatty acids of beef or pork fat, but only 4-5% of those in vegetable oils. Stearic acid seems not to increase LDL-cholesterol levels.Elevated Palmitic Acid (16:0)
Palmitic acid content has proven to be remarkably plastic in soybean, with ranges from ∼4% to levels that exceed 40% of total seed oil. A number of different genes and genetic mutations are associated with elevated levels of palmitic acid, and at least five independent loci have been implicated. These include fap2 (Erickson et al., 1988), fap4 (Schnebly et al., 1994), fap5 (Stoltzfus et al., 2000a), fap6 (Narvel et al., 2000), fap7 (Stoltzfus et al., 2000b), and sop2 (Takagi et al., 1995). The allelic status of the sop2 gene to the others in this series is currently unclear.
The molecular genetic basis for the elevated palmitic content in EMS-induced line C1727 (fap2) has been determined to be due to a nonsense mutation that prematurely terminates the open reading frame of a 3-keto-acyl-ACP synthase II (KASII) gene (Figure 5.1) (Aghoram et al., 2006). Another, independent fap2 mutant from line A-19 was generated by NMU mutagenesis, though the exact genetic basis has not been reported (Fehr et al., 1991). The molecular genetic basis for genes involved in elevated palmitic acid for the other genes in this allelic series have not been determined. Although considerable work has gone into the development of mutant resources for elevated palmitic acid content, no commercial cultivars with elevated palmitic acid content have been released (Fehr, 2007).Palmitoylated Proteins
Palmitic acid (16:0) is covalently added to a membrane protein through a thiolate side chain of cysteine residues (Fig. 6.11) [26]. The reaction is catalyzed by palmitoyl acyl transferases which uses palmitoyl-CoA as the substrate and generates a reversible thio-ester. Therefore, the protein is S-palmitoylated. Because palmitic acid is two carbons longer than myristic acid, it is more hydrophobic and thus its anchor to the membrane is considerably stronger and, without enzymatic intervention, is almost permanent. S-palmitoylation is often used to strengthen other types of lipidations, such as myristoylation or prenylation, and selectively concentrates in lipid rafts. The thio-ester attachment is readily cleaved by thio-esterases. Palmitoylation reversibility is only caused by acyl-transferases and thio-esterases. This stands in sharp contrast to myristoylation and prenylation that are weakly bound but not hydrolysable.Egg Yolk
Oleic acid, palmitic acid, and linoleic acid, in that order, consist of nearly 90 mol% of all fatty acids in triacylglycerols of egg yolk (Table 6). According to Gornall and Kuksis, the most common triacylglycerol species of egg yolk are 16:0-18:1-18:1 (29 mol%), 16:0-18:2-18:1 (15 mol%), 18:1-18:2-18:1 (7 mol%), and 16:0-18:1-18:0 (7 mol%). Palmitic and linoleic acids are very unevenly distributed between the sn-positions: over 70% of 16:0 and 18:2 is in the sn-1 and sn-2 position, respectively. Stearic acid is evenly distributed between the primary positions and oleic acid between the sn-2 and sn-3 positions. Metabolism and Nomenclature
Palmitic acid and stearic acid are the major products of fatty acid synthase. Both of these fatty acids are saturated; that is, they contain no double bonds between adjacent carbons. "Saturated" means that they contain a maximal content of hydrogen atoms. Although palmitate is a major fatty acid in cell membranes, most or all membranes contain longer-chain fatty acids as well. These fatty acids, having from 18 to 22 carbon atoms, are synthesized by the fatty acyl chain elongation system. The chain elongation system is located primarily in the endoplasmic reticulum, in contrast to fatty acid synthase, which is cytosolic. The chain elongation system catalyzes the addition of 2-carbon units to the growing fatty acid.
Mammalian Desaturases
In addition to chain elongation, fatty acids are modified by the introduction of double bonds (desaturation). Enzymes, called desaturases, catalyze the synthesis of unsaturated fatty acids. They can use saturated or partially unsaturated fatty acids as substrates. Δ9-Desaturase, for example, catalyzes the introduction of a double bond between carbons 9 and 10 of a fatty acid (counting from the carboxylic acid end). Three examples of reactions of Δ-desaturases are shown in Figure 9.95.
Name Palmitic Acid
Accession Number DB03796 (EXPT01393, EXPT02607)
Type Small Molecule
Groups Approved
A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.
Is the Palmitic Acid in Coconut Oil Unhealthy?
You may or may not have seen palmitic acid listed on food ingredient labels. That's because if coconut oil or palm oil are on the ingredient list, the food may very well have palmitic acid and not label it. This fatty acid is found in animal products and some plant oils.
So, what is palmitic acid and what are its possible health effects?
Palmitic acid is a saturated fat. It's naturally found in some animal products like meat and dairy, as well as in palm and coconut oils. Because these two oils are frequently used in processed foods, you might be getting palmitic acid in your diet without even realizing it.
Chemical Taxonomy
Description: belongs to the class of organic compounds known as long-chain fatty acids. These are fatty acids with an aliphatic tail that contains between 13 and 21 carbon atoms.
Kingdom Organic compounds 
Super Class: Lipids and lipid-like molecules 
Class: Fatty Acyls 
Sub Class: Fatty acids and conjugates 
Direct Parent: Long-chain fatty acids 
Alternative Parents 
Straight chain fatty acids 
Monocarboxylic acids and derivatives 
Carboxylic acids 
Organic oxides 
Hydrocarbon derivatives 
Carbonyl compounds 
Long-chain fatty acid
Straight chain fatty acid
Monocarboxylic acid or derivatives
Carboxylic acid
Carboxylic acid derivative
Organic oxygen compound
Organic oxide
Hydrocarbon derivative
Organooxygen compound
Carbonyl group
Aliphatic acyclic compound
Molecular Framework Aliphatic acyclic compounds
External Descriptors 
long-chain fatty acid (CHEBI:15756 )
straight-chain saturated fatty acid (CHEBI:15756 )
Straight chain fatty acids (C00249 )
Saturated fatty acids (C00249 )
Straight chain fatty acids (LMFA01010001 )
Physical Properties
State Solid
Charge 0
Melting point 61.8 °C
Biological Properties
Cellular Locations 
Cell Envelope, Cytoplasm, Endoplasmic Reticulum, Extracellular, Lipid Particle, Mitochondrion, Peroxisome



SMPDB Reactions 
Palmitic acid + Adenosine triphosphate + Coenzyme A → Adenosine monophosphate + Pyrophosphate + Palmityl-CoA
PA(16:0/0:0) + Palmitic acid → PA(16:0/16:0) + Coenzyme A
Trans-Hexa-dec-2-enoic acid → Palmitic acid
Palmitic acid + Adenosine triphosphate + Coenzyme A → Palmityl-CoA + Adenosine monophosphate + Pyrophosphate
Palmityl-CoA + water → Palmitic acid + Coenzyme A



KEGG Reactions 
myristic acid + malonyl-CoA + hydron + NADPH → Carbon dioxide + NADP + water + Coenzyme A + Palmitic acid
malonyl-CoA + hydron + NADPH + Palmitic acid → stearic acid + Carbon dioxide + NADP + water + Coenzyme A
hydron + malonyl-CoA + oxygen + NADPH + Palmitic acid → NADP + Carbon dioxide + Coenzyme A + Oleic acid + water
Adenosine triphosphate + Coenzyme A + Palmitic acid ↔ Adenosine monophosphate + Pyrophosphate + Palmityl-CoA
water + palmitoyl-[acyl-carrier protein] ↔ acyl-carrier protein + hydron + Palmitic acid



Palmitic Acid in Cell Culture
Importance and uses of palmitic acid in serum-free eukaryotic, including hybridoma and Chinese Hamster Ovary (CHO) cell, cultures
Palmitic Acid, a Serum-Free Medium Supplement, Useful In Biomanufacturing; Tissue Engineering and Specialty Media:
Fatty acids of the n-3, n-6 and n-9 families are important supplements for cell culture systems. They are important in cell culture systems used to biomanufacture heterologous proteins, such as monoclonal antibodies. Fatty acids have been shown to be important for the growth and productivity of Chinese Hamster Ovary (CHO) cells.
The n-9 family of fatty acids, including oleic acid, can be synthesized by animal cells from the saturated precursors palmitic and stearic acids. Historically, palmitic acid has been provided to cells in culture as a component of serum, albumin complex or esterified to molecules such as cholesterol. Palmitic acid is poorly soluble in aqueous media, but it is non-susceptible to peroxidation.Primary Functions of Palmitic Acid in Cell Culture Systems:
Long-term energy storage: energy derived from NADPH and ATP is stored in fatty acids. Fatty acids are esterified to a glycerol backbone to form a group of compounds known as mono-, di- and tri- glycerides (neutral fats). Energy is released when fatty acids are degraded.
Fatty acids are precursors of other molecules: prostaglandins, prostacyclins, thromboxanes, phospho-lipids, glycolipids, and vitamins.
Structural elements: fatty acids are important constituents of cell structures such as the membranesChemical Attributes of Palmitic Acid that make it a Useful Serum-Free Medium Supplement:
Fatty acids (FA) are long-chain carboxylic acids that are insoluble in water. These fatty acid chains can be from 4 to 30 carbons long, but physiologically the most important fatty acids are from 16 to 22 carbons long. Since fatty acids are synthesized naturally by the addition of acetyl groups, they have an even numbers of carbon atoms-C2, C4, etc. They can be saturated or unsaturated. Natural fatty acids have their double bonds in the cis-configuration and are usually esterified to glycerol backbones to form complex lipids. Fatty acids that contain more than one double bond are called polyunsaturated fatty acids (PUFAs).
In animals, most fatty acids with 16 or more carbons belong to one of three main fatty acid families. All unsaturated members of a family are n-3, n-6, or n-9. Members of these FA families are not inter-convertible. Palmitic acid family; palmitic acid is saturated, but unsaturated fatty acids derived from it are of the n-9 type. Animal cells can de novo synthesize palmitic fatty acid and its n-9 derivatives. However, de novo synthesis requires the utilization of energy. Palmitic acid (16:0) is a precursor of stearic acid (18:0). Palmitic acid can also be dehydrogenated to form palmitoleic acid (16:1, n-9). A number of other important fatty acids are derived from palmitoleic acid. In animal cells, oleic (18:1, n-9) acid is created by the dehydrogenation (desaturation) of stearic acid. Oleic acid is further elongated and desaturated into a family of n-9 fatty acids. If oleic acid is not provided in sufficient quantity, cells cannot produce other important fatty acids, and fatty acid derivatives.Palmitic Acid
Molecular FormulaC16H32O2
Average mass256.424 Da
Monoisotopic mass256.240234 Da
ChemSpider ID960



Palmitik asit
Palmitik asit (IUPAC adlandırma sisteminde hexadekanoic asit) hayvan ve bitkilerde bulunan en yaygın doymuş yağ asitidir. 16 karbonludur, baz haline palmitat denir. Ergime sıcaklığı 63.1 °C, kimyasal formülü CH3(CH2)14COOH'tür. İsminden de anlaşılacağı üzere palmiye ağacının yağından ve palmiye çekirdeğinde bulunur. Tereyağ, peynir, süt ve ette de bulunur.
Canlılarda yağ asitlerinin oluşumunda (lipojenez) ilk sentezlenen yağ asidi palmitik asittir, daha uzun yağ asitleri ondan üretilir. Asetil-KoA karboksilaz enzimi asetil-ACP'yi malonil-ACP'ye dönüştürür, palmitat bu enzim üzerinde negatif geribesleme yaparak daha fazla palmitat üretimini engeller.
Palmitik asit bir karboksilik asit olduğu için çeşitli organik alkollerle esterleşebilir. Düşük yağlı süt üretiminde sütten alınan yağla beraber kaybolan A vitamininin (retinol) yerini almak için retinol ile palmitatın esterleşmiş hali olan retinil palmitat geri eklenir. Kozmetik sanayisinde de A vitamini içeren kremlerde de retinil palmitat bulunur. İlaç sanayisinde palmitatla esterleşmiş bazı ilaçlar, örneğin kloramfenikol palmitat, etkisizdirler, ince bağırsakta hidroliz olduktan sonra aktif hale dönüşürler. Gıda sanayinde yağların bozulmasını engellemek için kullanılan askorbil palmitat askorbik asitin antioksidan özelliği ile palmitatın yağda çözünürlüğünü birleştirir
Hücre zarında bulunan bazı proteinlerin sistein gruplarında palmitat bağlıdır, bu sayede protein zara takılı kalır.
Palmitik asit türevleri II. Dünya Savaşı sırasında napalm üretiminde kullanılmışlardır.
Palmitik asitin indirgenmesi sonucunda palmitil alkol oluşur.
Tanımı: Beyaz kristal katı.
Ambalaj birimi: 25 kg.
CAS No: 57-10-3
Kimyasal adı: Hekzadekanoik asit; hekzadesilik asit.
Asit değeri: 219 mg KOH/g
İyod değeri, I2: % 0,2
Titer: 61,7 oC
Renk, Lovibond 5 ¼: 0,1 R, 0,7 Y
Renk, APHA: 30
Molekül ağırlığı: 256,22 g/mol
Zincir dağılımı C14: % 0,7
Sabunlaşma değeri: 217-223 mgKOH/g
C16: % 98,9
Su içeriği: < % 0,2
C18: % 0,5
Özellikleri: Bitki ve hayvanlarda bulunan doymuş yağ asidi grubunun 16 karbonlu üyesidir. İlk olarak palm yağından elde edilmiştir. Geniş dağılımına rağmen yağlarda çok büyük oranlarda bulunmamaktadır. Genellikle toplam yağ asidinin % 5'ini oluşturur, bilinen bitkisel yağlarda (yerfıstığı yağı, soya, mısır, Hindistan cevizi yağı) % 10 kadar ve deniz hayvanlarında bulunur. Domuz yağı, don yağı, kakao, tereyağı, palm yağı bu komponentin % 25-40'ını içerir. Renk ve oksidasyon stbilitesi iyidir. Alkalilerle olan tuzları suda stearik asidin tuzlarından daha fazla erir.
Kullanım alanları: Kozmetiklerde, wax formülasyonlarında ve mumlarda geniş kullanım alanı bulmaktadır. Emülsifiyerlerin üretimi, anyonik ve non iyonik yüzey aktiflerin üretimi, tekstil kimyasalları ve sabun-deterjan üretiminde kullanılmaktadır. Ayrıca gıdalarda topaklanmayı önleyici olarak da kullanılmakta ve bakteri karşıtı etkisinden yararlanılmaktadır.
Depolama: 60 oC'nin altında yaklaşık 2 yıl stabildir.
Hayvansal yağlarda bulunan doymamış yağ asitlerinden biri 16 karbon atomu ve 1 doymamış bağa sahip olan palmitoleik asittir.
Palmitoleik asit, kapalı formülü C16H30O2, mol kütlesi 254.408 kg/mol, yoğunluğu 0.894 g/cm3 ve erime noktası -0.1°C olan tekli doymamış yağ asididir.. Geometrik izomeri, çift bağlar ucundaki karbon atomlarına bağlı hidrojen atomlarının konfigürasyonuna göre şekillenen palmitoleik asidin; cis ve trans olarak iki izomeri bulunmaktadır. Hidrojen atomları karbon zincirinin aynı tarafında ise cis, aksi yönlerde ise trans izomerler ortaya çıkmakta (Şekil 1) ve pozisyon izomerisi ise, molekül içinde çift bağların yer değiştirmesi ile oluşmaktadır (Mensink ve Katan, 1990).



Ataman Chemicals © 2015 All Rights Reserved.