Exact Mass: 732.614492

Exact Mass Matches: 732.614492

Found 500 metabolites which its exact mass value is equals to given mass value 732.614492, within given mass tolerance error 0.05 dalton. Try search metabolite list with more accurate mass tolerance error 0.01 dalton.

2,3-di-O-Phytanyl-sn-glycerol phosphate

2,3-bis-O-phytanyl-sn-glycerol 1-phosphate

C43H89O6P (732.6396424)

SM(d36:0)

(2-{[(2S,3R)-3-hydroxy-2-octadecanamidooctadecyl phosphonato]oxy}ethyl)trimethylazanium

C41H85N2O6P (732.614492)

Sphingomyelin (d18:0/18:0) or SM(d18:0/18:0) is a type of sphingolipid found in animal cell membranes, especially in the membranous myelin sheath which surrounds some nerve cell axons. It usually consists of phosphorylcholine and ceramide. In humans, sphingomyelin is the only membrane phospholipid not derived from glycerol. Like all sphingolipids, SPH has a ceramide core (sphingosine bonded to a fatty acid via an amide linkage). In addition it contains one polar head group, which is either phosphocholine or phosphoethanolamine. The plasma membrane of cells is highly enriched in sphingomyelin and is considered largely to be found in the exoplasmic leaflet of the cell membrane. However, there is some evidence that there may also be a sphingomyelin pool in the inner leaflet of the membrane. Moreover, neutral sphingomyelinase-2 - an enzyme that breaks down sphingomyelin into ceramide has been found to localise exclusively to the inner leaflet further suggesting that there may be sphingomyelin present there. Sphingomyelin can accumulate in a rare hereditary disease called Niemann-Pick Disease, types A and B. Niemann-Pick disease is a genetically-inherited disease caused by a deficiency in the enzyme Sphingomyelinase, which causes the accumulation of Sphingomyelin in spleen, liver, lungs, bone marrow, and the brain, causing irreversible neurological damage. SMs play a role in signal transduction. Sphingomyelins are synthesized by the transfer of phosphorylcholine from phosphatidylcholine to a ceramide in a reaction catalyzed by sphingomyelin synthase. Sphingomyelin (d18:0/18:0) or SM(d18:0/18:0)is a type of sphingolipid found in animal cell membranes, especially in the membranous myelin sheath which surrounds some nerve cell axons. It usually consists of phosphorylcholine and ceramide. In humans, sphingomyelin is the only membrane phospholipid not derived from glycerol. Like all sphingolipids, SPH has a ceramide core (sphingosine bonded to a fatty acid via an amide linkage). In addition it contains one polar head group, which is either phosphocholine or phosphoethanolamine. The plasma membrane of cells is highly enriched in sphingomyelin and is considered largely to be found in the exoplasmic leaflet of the cell membrane. However, there is some evidence that there may also be a sphingomyelin pool in the inner leaflet of the membrane. Moreover, neutral sphingomyelinase-2 - an enzyme that breaks down sphingomyelin into ceramide has been found to localise exclusively to the inner leaflet further suggesting that there may be sphingomyelin present there. Sphingomyelin can accumulate in a rare hereditary disease called Niemann-Pick Disease, types A and B. Niemann-Pick disease is a genetically-inherited disease caused by a deficiency in the enzyme Sphingomyelinase, which causes the accumulation of Sphingomyelin in spleen, liver, lungs, bone marrow, and the brain, causing irreversible neurological damage. SMs play a role in signal transduction.

TG(15:0/14:1(9Z)/14:1(9Z))

1-Pentadecanoyl-2-(9Z-tetradecenoyl)-3-(9Z-tetradecenoyl)-glycerol

C46H84O6 (732.6267564)

TG(15:0/14:1(9Z)/14:1(9Z)) is a dimyristoleic acid triglyceride. Triglycerides (TGs or TAGs) are also known as triacylglycerols or triacylglycerides, meaning that they are glycerides in which the glycerol is esterified with three fatty acid groups (i.e. fatty acid trimesters of glycerol). TGs may be divided into three general types with respect to their acyl substituents. They are simple or monoacid if they contain only one type of fatty acid, diacid if they contain two types of fatty acids and triacid if three different acyl groups. Chain lengths of the fatty acids in naturally occurring triglycerides can be of varying lengths and saturations but 16, 18 and 20 carbons are the most common. TG(15:0/14:1(9Z)/14:1(9Z)), in particular, consists of one chain of pentadecanoic acid at the C-1 position, one chain of myristoleic acid at the C-2 position and one chain of myristoleic acid at the C-3 position. TGs are the main constituent of vegetable oil and animal fats. TGs are major components of very low density lipoprotein (VLDL) and chylomicrons, play an important role in metabolism as energy sources and transporters of dietary fat. They contain more than twice the energy (9 kcal/g) of carbohydrates and proteins. In the intestine, triglycerides are split into glycerol and fatty acids (this process is called lipolysis) with the help of lipases and bile secretions, which can then move into blood vessels. The triglycerides are rebuilt in the blood from their fragments and become constituents of lipoproteins, which deliver the fatty acids to and from fat cells among other functions. Various tissues can release the free fatty acids and take them up as a source of energy. Fat cells can synthesize and store triglycerides. When the body requires fatty acids as an energy source, the hormone glucagon signals the breakdown of the triglycerides by hormone-sensitive lipase to release free fatty acids. As the brain cannot utilize fatty acids as an energy source, the glycerol component of triglycerides can be converted into glucose for brain fuel when it is broken down. (www.cyberlipid.org, www.wikipedia.org)
TAGs can serve as fatty acid stores in all cells, but primarily in adipocytes of adipose tissue. The major building block for the synthesis of triacylglycerides, in non-adipose tissue, is glycerol. Adipocytes lack glycerol kinase and so must use another route to TAG synthesis. Specifically, dihydroxyacetone phosphate (DHAP), which is produced during glycolysis, is the precursor for TAG synthesis in adipose tissue. DHAP can also serve as a TAG precursor in non-adipose tissues, but does so to a much lesser extent than glycerol. The use of DHAP for the TAG backbone depends on whether the synthesis of the TAGs occurs in the mitochondria and ER or the ER and the peroxisomes. The ER/mitochondria pathway requires the action of glycerol-3-phosphate dehydrogenase to convert DHAP to glycerol-3-phosphate. Glycerol-3-phosphate acyltransferase then esterifies a fatty acid to glycerol-3-phosphate thereby generating lysophosphatidic acid. The ER/peroxisome reaction pathway uses the peroxisomal enzyme DHAP acyltransferase to acylate DHAP to acyl-DHAP which is then reduced by acyl-DHAP reductase. The fatty acids that are incorporated into TAGs are activated to acyl-CoAs through the action of acyl-CoA synthetases. Two molecules of acyl-CoA are esterified to glycerol-3-phosphate to yield 1,2-diacylglycerol phosphate (also known as phosphatidic acid). The phosphate is then removed by phosphatidic acid phosphatase (PAP1), to generate 1,2-diacylglycerol. This diacylglycerol serves as the substrate for addition of the third fatty acid to make TAG. Intestinal monoacylglycerols, derived from dietary fats, can also serve as substrates for the synthesis of 1,2-diacylglycerols.

TG(14:1(9Z)/15:0/14:1(9Z))

1-(9Z-Tetradecenoyl)-2-pentadecanoyl-3-(9Z-tetradecenoyl)-glycerol

C46H84O6 (732.6267564)

TG(14:1(9Z)/15:0/14:1(9Z)) is a dimyristoleic acid triglyceride. Triglycerides (TGs or TAGs) are also known as triacylglycerols or triacylglycerides, meaning that they are glycerides in which the glycerol is esterified with three fatty acid groups (i.e. fatty acid trimesters of glycerol). TGs may be divided into three general types with respect to their acyl substituents. They are simple or monoacid if they contain only one type of fatty acid, diacid if they contain two types of fatty acids and triacid if three different acyl groups. Chain lengths of the fatty acids in naturally occurring triglycerides can be of varying lengths and saturations but 16, 18 and 20 carbons are the most common. TG(14:1(9Z)/15:0/14:1(9Z)), in particular, consists of one chain of myristoleic acid at the C-1 position, one chain of pentadecanoic acid at the C-2 position and one chain of myristoleic acid at the C-3 position. TGs are the main constituent of vegetable oil and animal fats. TGs are major components of very low density lipoprotein (VLDL) and chylomicrons, play an important role in metabolism as energy sources and transporters of dietary fat. They contain more than twice the energy (9 kcal/g) of carbohydrates and proteins. In the intestine, triglycerides are split into glycerol and fatty acids (this process is called lipolysis) with the help of lipases and bile secretions, which can then move into blood vessels. The triglycerides are rebuilt in the blood from their fragments and become constituents of lipoproteins, which deliver the fatty acids to and from fat cells among other functions. Various tissues can release the free fatty acids and take them up as a source of energy. Fat cells can synthesize and store triglycerides. When the body requires fatty acids as an energy source, the hormone glucagon signals the breakdown of the triglycerides by hormone-sensitive lipase to release free fatty acids. As the brain cannot utilize fatty acids as an energy source, the glycerol component of triglycerides can be converted into glucose for brain fuel when it is broken down. (www.cyberlipid.org, www.wikipedia.org)
TAGs can serve as fatty acid stores in all cells, but primarily in adipocytes of adipose tissue. The major building block for the synthesis of triacylglycerides, in non-adipose tissue, is glycerol. Adipocytes lack glycerol kinase and so must use another route to TAG synthesis. Specifically, dihydroxyacetone phosphate (DHAP), which is produced during glycolysis, is the precursor for TAG synthesis in adipose tissue. DHAP can also serve as a TAG precursor in non-adipose tissues, but does so to a much lesser extent than glycerol. The use of DHAP for the TAG backbone depends on whether the synthesis of the TAGs occurs in the mitochondria and ER or the ER and the peroxisomes. The ER/mitochondria pathway requires the action of glycerol-3-phosphate dehydrogenase to convert DHAP to glycerol-3-phosphate. Glycerol-3-phosphate acyltransferase then esterifies a fatty acid to glycerol-3-phosphate thereby generating lysophosphatidic acid. The ER/peroxisome reaction pathway uses the peroxisomal enzyme DHAP acyltransferase to acylate DHAP to acyl-DHAP which is then reduced by acyl-DHAP reductase. The fatty acids that are incorporated into TAGs are activated to acyl-CoAs through the action of acyl-CoA synthetases. Two molecules of acyl-CoA are esterified to glycerol-3-phosphate to yield 1,2-diacylglycerol phosphate (also known as phosphatidic acid). The phosphate is then removed by phosphatidic acid phosphatase (PAP1), to generate 1,2-diacylglycerol. This diacylglycerol serves as the substrate for addition of the third fatty acid to make TAG. Intestinal monoacylglycerols, derived from dietary fats, can also serve as substrates for the synthesis of 1,2-diacylglycerols.

CE(MonoMe(13,5))

2,15-dimethyl-14-(6-methylheptan-2-yl)tetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadec-7-en-5-yl 13-(3-methyl-5-pentylfuran-2-yl)tridecanoate

C50H84O3 (732.6420114)

CE(MonoMe(13,5)) is a cholesterol fatty acid ester or simply a cholesterol ester (CE). Cholesterol esters are cholesterol molecules with long-chain fatty acids linked to the hydroxyl group. They are much less polar than free cholesterol and appear to be the preferred form for transport in plasma and for storage. Cholesterol esters do not contribute to membranes but are packed into intracellular lipid particles or lipoprotein particles. Because of the mechanism of synthesis, plasma cholesterol esters tend to contain relatively high proportions of C18 fatty acids. Cholesterol esters are major constituents of the adrenal glands and they also accumulate in the fatty lesions of atherosclerotic plaques. Cholesterol esters are also major constituents of the lipoprotein particles carried in blood (HDL, LDL, VLDL). The cholesterol esters in high-density lipoproteins (HDL) are synthesized largely by transfer of fatty acids to cholesterol from position sn-2 (or C-2) of phosphatidylcholine catalyzed by the enzyme lecithin cholesterol acyl transferase (LCAT). The enzyme also promotes the transfer of cholesterol from cells to HDL. As cholesterol esters accumulate in the lipoprotein core, cholesterol is removed from its surface thus promoting the flow of cholesterol from cell membranes into HDL. This in turn leads to morphological changes in HDL, which grow and become spherical. Subsequently, cholesterol esters are transferred to the other lipoprotein fractions LDL and VLDL, a reaction catalyzed by cholesteryl ester transfer protein. Another enzyme, acyl-CoA:cholesterol acyltransferase (ACAT) synthesizes cholesterol esters from CoA esters of fatty acids and cholesterol. Cholesterol ester hydrolases liberate cholesterol and free fatty acids when required for membrane and lipoprotein formation, and they also provide cholesterol for hormone synthesis in adrenal cells.

CE(11D6)

[10,13-dimethyl-17-(6-methylheptan-2-yl)-2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl] 11-(5-hexyl-3,4-dimethylfuran-2-yl)undecanoate

C50H84O3 (732.6420114)

CE(11D6) is a furan fatty acid ester of cholesterol or simply a cholesteryl ester (CE). Cholesteryl esters are much less polar than free cholesterol and appear to be the preferred form for transport in plasma and for storage. Cholesteryl esters do not contribute to membranes but are packed into intracellular lipid particles or lipoprotein particles. Because of the mechanism of synthesis, plasma cholesteryl esters tend to contain relatively high proportions of C18 fatty acids. Cholesteryl esters are major constituents of the adrenal glands and they also accumulate in the fatty lesions of atherosclerotic plaques. Cholesteryl esters are also major constituents of the lipoprotein particles carried in blood (HDL, LDL, VLDL). The cholesteryl esters in high-density lipoproteins (HDL) are synthesized largely by transfer of fatty acids to cholesterol from position sn-2 (or C-2) of phosphatidylcholine catalyzed by the enzyme lecithin cholesterol acyl transferase (LCAT). The enzyme also promotes the transfer of cholesterol from cells to HDL. As cholesteryl esters accumulate in the lipoprotein core, cholesterol is removed from its surface thus promoting the flow of cholesterol from cell membranes into HDL. This in turn leads to morphological changes in HDL, which grow and become spherical. Subsequently, cholesteryl esters are transferred to the other lipoprotein fractions LDL and VLDL, a reaction catalyzed by cholesteryl ester transfer protein. Another enzyme, acyl-CoA:cholesterol acyltransferase (ACAT) synthesizes cholesteryl esters from CoA esters of fatty acids and cholesterol. Cholesteryl ester hydrolases liberate cholesterol and free fatty acids when required for membrane and lipoprotein formation, and they also provide cholesterol for hormone synthesis in adrenal cells. The shorthand notation for CE(11D6) refers to the furan fatty acids 11-carbon carboxyalkyl moiety, the dimethyl substitutions in the 3- and 4-positions of its furan moiety, and its 6-carbon alkyl moiety.

CE(11M7)

[10,13-dimethyl-17-(6-methylheptan-2-yl)-2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl] 11-(5-heptyl-3-methylfuran-2-yl)undecanoate

C50H84O3 (732.6420114)

CE(11M7) is a furan fatty acid ester of cholesterol or simply a cholesteryl ester (CE). Cholesteryl esters are much less polar than free cholesterol and appear to be the preferred form for transport in plasma and for storage. Cholesteryl esters do not contribute to membranes but are packed into intracellular lipid particles or lipoprotein particles. Because of the mechanism of synthesis, plasma cholesteryl esters tend to contain relatively high proportions of C18 fatty acids. Cholesteryl esters are major constituents of the adrenal glands and they also accumulate in the fatty lesions of atherosclerotic plaques. Cholesteryl esters are also major constituents of the lipoprotein particles carried in blood (HDL, LDL, VLDL). The cholesteryl esters in high-density lipoproteins (HDL) are synthesized largely by transfer of fatty acids to cholesterol from position sn-2 (or C-2) of phosphatidylcholine catalyzed by the enzyme lecithin cholesterol acyl transferase (LCAT). The enzyme also promotes the transfer of cholesterol from cells to HDL. As cholesteryl esters accumulate in the lipoprotein core, cholesterol is removed from its surface thus promoting the flow of cholesterol from cell membranes into HDL. This in turn leads to morphological changes in HDL, which grow and become spherical. Subsequently, cholesteryl esters are transferred to the other lipoprotein fractions LDL and VLDL, a reaction catalyzed by cholesteryl ester transfer protein. Another enzyme, acyl-CoA:cholesterol acyltransferase (ACAT) synthesizes cholesteryl esters from CoA esters of fatty acids and cholesterol. Cholesteryl ester hydrolases liberate cholesterol and free fatty acids when required for membrane and lipoprotein formation, and they also provide cholesterol for hormone synthesis in adrenal cells. The shorthand notation for CE(11M7) refers to the furan fatty acids 11-carbon carboxyalkyl moiety, the methyl substitution in the 3-position of its furan moiety, and its 7-carbon alkyl moiety.

CE(12D5)

[10,13-dimethyl-17-(6-methylheptan-2-yl)-2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl] 12-(3,4-dimethyl-5-pentylfuran-2-yl)dodecanoate

C50H84O3 (732.6420114)

CE(12D5) is a furan fatty acid ester of cholesterol or simply a cholesteryl ester (CE). Cholesteryl esters are much less polar than free cholesterol and appear to be the preferred form for transport in plasma and for storage. Cholesteryl esters do not contribute to membranes but are packed into intracellular lipid particles or lipoprotein particles. Because of the mechanism of synthesis, plasma cholesteryl esters tend to contain relatively high proportions of C18 fatty acids. Cholesteryl esters are major constituents of the adrenal glands and they also accumulate in the fatty lesions of atherosclerotic plaques. Cholesteryl esters are also major constituents of the lipoprotein particles carried in blood (HDL, LDL, VLDL). The cholesteryl esters in high-density lipoproteins (HDL) are synthesized largely by transfer of fatty acids to cholesterol from position sn-2 (or C-2) of phosphatidylcholine catalyzed by the enzyme lecithin cholesterol acyl transferase (LCAT). The enzyme also promotes the transfer of cholesterol from cells to HDL. As cholesteryl esters accumulate in the lipoprotein core, cholesterol is removed from its surface thus promoting the flow of cholesterol from cell membranes into HDL. This in turn leads to morphological changes in HDL, which grow and become spherical. Subsequently, cholesteryl esters are transferred to the other lipoprotein fractions LDL and VLDL, a reaction catalyzed by cholesteryl ester transfer protein. Another enzyme, acyl-CoA:cholesterol acyltransferase (ACAT) synthesizes cholesteryl esters from CoA esters of fatty acids and cholesterol. Cholesteryl ester hydrolases liberate cholesterol and free fatty acids when required for membrane and lipoprotein formation, and they also provide cholesterol for hormone synthesis in adrenal cells. The shorthand notation for CE(12D5) refers to the furan fatty acids 12-carbon carboxyalkyl moiety, the dimethyl substitutions in the 3- and 4-positions of its furan moiety, and its 5-carbon alkyl moiety.

DG(22:0/20:4(6Z,8E,10E,14Z)-2OH(5S,12R)/0:0)

(2S)-2-{[(5R,6Z,8E,10E,12S,14Z)-5,12-dihydroxyicosa-6,8,10,14-tetraenoyl]oxy}-3-hydroxypropyl docosanoic acid