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2-Oleoyl Glycerol

(Synonyms: 2-十八烯酸单甘油酯;2-甘油单油酸酯) 目录号 : GC40406

A natural monoacylglycerol

2-Oleoyl Glycerol Chemical Structure

Cas No.:3443-84-3

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1mg
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5mg
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10mg
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25mg
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产品描述

2-Oleoyl glycerol (2-OG) is a natural monoacylglycerol with an 18:1 oleoyl group at the sn-2 position of glycerol. 2-OG, like 2-arachidonoyl glycerol , is metabolized by monoacylglycerol lipase, but, unlike 2-AG, it is not metabolized by cyclooxygenases or lipoxygenases.[1][2][3]  2-OG is an agonist of GPR119 (EC50 = 2.5 µM), stimulating the release of glucagon-like peptide-1 from intestinal L-cells. [4] 

Reference:
[1]. Brengdahl, J., and Fowler, C.J. A novel assay for monoacylglycerol hydrolysis suitable for high-throughput screening. Analytical Biochemistry 359, 40-44 (2006).
[2]. Ghafouri, N., Tiger, G., Razdan, R.K., et al. Inhibition of monoacylglycerol lipase and fatty acid amide hydrolase by analogues of 2-arachidonoylglycerol. British Journal of Pharmacology 143, 774-784 (2004).
[3]. Woodhams, S.G., Wong, A., Barrett, D.A., et al. Spinal administration of the monoacylglycerol lipase inhibitor JZL184 produces robust inhibitory effects on nociceptive processing and the development of central sensitization in the rat. Brit.J.Pharmacol. 167, 1609-1619 (2012).
[4]. Hansen, K.B., Rosenkilde, M.M., Knop, F.K., et al. 2-Oleoyl glycerol is a GRP119 agonist and signals GLP-1 release in humans. Journal of Clinical Endocrinology and Metabolism 96(9), E1409-E1417 (2011).

Chemical Properties

Cas No. 3443-84-3 SDF
别名 2-十八烯酸单甘油酯;2-甘油单油酸酯
化学名 2-hydroxy-1-(hydroxymethyl)ethyl ester-9Z-octadecenoic acid
Canonical SMILES CCCCCCCC/C=C\CCCCCCCC(OC(CO)CO)=O
分子式 C21H40O4 分子量 356.5
溶解度 10 mg/ml in DMSO, 10 mg/ml in DMF, 15 mg/ml in Ethanol 储存条件 Store at -80°C, protect from light
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1 mg 5 mg 10 mg
1 mM 2.805 mL 14.0252 mL 28.0505 mL
5 mM 0.561 mL 2.805 mL 5.6101 mL
10 mM 0.2805 mL 1.4025 mL 2.805 mL
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Research Update

2-Oleoyl Glycerol is a GPR119 agonist and signals GLP-1 release in humans

J Clin Endocrinol Metab 2011 Sep;96(9):E1409-17.PMID:21778222DOI:10.1210/jc.2011-0647.

Objective: Dietary fat is thought to stimulate release of incretin hormones via activation of fatty acid receptors in the intestine. However, dietary fat (triacylglycerol) is digested to 2-monoacylglycerol and fatty acids. Activation of G protein-coupled receptor 119 (GPR119) stimulates glucagon-like peptide-1 (GLP-1) release from the intestinal L-cells. We aimed to investigate if 2-Oleoyl Glycerol (2OG) can activate GPR119 in vitro and stimulate GLP-1 secretion in vivo. Research design and methods: Agonist activity for various lipids was tested on transiently expressed human GPR119 in COS-7 cells. The effect of a jejunal bolus of 2 g 2OG on plasma levels of GLP-1 was evaluated in eight healthy human volunteers. The effect of 2OG was compared to an equimolar amount of oleic acid, a degradation product from 2OG, and the vehicle, glycerol. Digestion of 5 ml olive oil with pancreatic lipase will result in formation of approximately 2 g 2OG and 3.2 g oleic acid. Results: 2OG and other 2-monoacylglycerols increased intracellular concentrations of cAMP in GPR119-expressing COS-7 cells (2OG EC(50) = 2.5 μm). Administration of 2OG to humans significantly increased plasma GLP-1 (0-25 min) when compared to the two controls, oleic acid and vehicle. Plasma levels of glucose-dependent insulinotropic polypeptide also increased. Conclusion: 2OG and other 2-monoacylglycerols formed during fat digestion can activate GPR119 and cause incretin release from the human intestine. This mechanism is likely to contribute to the known stimulatory effect of dietary fat on incretin secretion, and it indicates that GPR119 is a fat sensor.

Comparing olive oil and C4-dietary oil, a prodrug for the GPR119 agonist, 2-Oleoyl Glycerol, less energy intake of the latter is needed to stimulate incretin hormone secretion in overweight subjects with type 2 diabetes

Nutr Diabetes 2018 Jan 12;8(1):2.PMID:29330461DOI:10.1038/s41387-017-0011-z.

Background/objective: After digestion, dietary triacylglycerol stimulates incretin release in humans, mainly through generation of 2-monoacylglycerol, an agonist for the intestinal G protein-coupled receptor 119 (GPR119). Enhanced incretin release may have beneficial metabolic effects. However, dietary fat may promote weight gain and should therefore be restricted in obesity. We designed C4-dietary oil (1,3-di-butyryl-2-oleoyl glycerol) as a 2-Oleoyl Glycerol (2-OG)-generating fat type, which would stimulate incretin release to the same extent while providing less calories than equimolar amounts of common triglycerides, e.g., olive oil. Subjects and methods: We studied the effect over 180 min of (a) 19 g olive oil plus 200 g carrot, (b) 10.7 g C4 dietary oil plus 200 g carrot and (c) 200 g carrot, respectively, on plasma responses of gut and pancreatic hormones in 13 overweight patients with type 2 diabetes (T2D). Theoretically, both oil meals result in formation of 7.7 g 2-OG during digestion. Results: Both olive oil and C4-dietary oil resulted in greater postprandial (P ≤ 0.01) glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) responses (incremental area under curve (iAUC)): iAUCGLP-1: 645 ± 194 and 702 ± 97 pM × min; iAUCGIP: 4,338 ± 764 and 2,894 ± 601 pM × min) compared to the carrot meal (iAUCGLP-1: 7 ± 103 pM × min; iAUCGIP: 266 ± 234 pM × min). iAUC for GLP-1 and GIP were similar for C4-dietary oil and olive oil, although olive oil resulted in a higher peak value for GIP than C4-dietary oil. Conclusion: C4-dietary oil enhanced secretion of GLP-1 and GIP to almost the same extent as olive oil, in spite of liberation of both 2-OG and oleic acid, which also may stimulate incretin secretion, from olive oil. Thus, C4-dietary oil is more effective as incretin releaser than olive oil per unit of energy and may be useful for dietary intervention.

GPR119 as a fat sensor

Trends Pharmacol Sci 2012 Jul;33(7):374-81.PMID:22560300DOI:10.1016/j.tips.2012.03.014.

The GPR119 receptor is expressed predominantly in pancreatic β cells and in enteroendocrine cells. It is a major target for the development of anti-diabetic drugs that through GPR119 activation may stimulate both insulin and GLP-1 release. GPR119 can be activated by oleoylethanolamide and several other endogenous lipids containing oleic acid: these include N-oleoyl-dopamine, 1-oleoyl-lysophosphatidylcholine, generated in the tissue, and 2-Oleoyl Glycerol generated in the gut lumen. Thus, the well-known stimulation of GLP-1 release by dietary fat is probably not only mediated by free fatty acids acting through, for example, GPR40, but is also probably mediated in large part through the luminal formation of 2-monoacylglycerol acting on the 'fat sensor' GPR119. In the pancreas GPR119 may also be stimulated by 2-monoacylglycerol generated from local turnover of pancreatic triacylglycerol. Knowledge about the endogenous physiological ligands and their mode of interaction with GPR119 will be crucial for the development of efficient second-generation modulators of this important drug target.

Endocannabinoids and diacylglycerol kinase activity

Biochim Biophys Acta 2011 Apr;1808(4):1050-3.PMID:21194521DOI:10.1016/j.bbamem.2010.12.022.

Mammalian diacylglycerol kinases are a family of enzymes that catalyze the phosphorylation of diacylglycerol to produce phosphatidic acid. The extent of interaction of these enzymes with monoacylglycerols is the focus of the present study. Because of the structural relationship between mono- and diacylglycerols, one might expect the monoacylglycerols to be either substrates or inhibitors of diacylglycerol kinases. This would have some consequence to lipid metabolism. One of the lipid metabolites that would be affected is 2-arachidonoyl glycerol, which is an endogenous ligand for the CB1 cannabinoid receptor. We determined if the monoglycerides 2-arachidonoyl glycerol or 2-Oleoyl Glycerol affected diacylglycerol kinase activity. We found that 2-arachidonoyl glycerol is a very poor substrate for either the epsilon or the zeta isoforms of diacylglycerol kinases. Moreover, 2-arachidonoyl glycerol is an inhibitor for both of these diacylglycerol kinase isoforms. 2-Oleoyl Glycerol is also a poor substrate for these two isoforms of diacylglycerol kinases. As an inhibitor, 2-Oleoyl Glycerol inhibits diacylglycerol kinase ε less than does 2-arachidonoyl glycerol, while for diacylglycerol kinase ζ, these two monoglycerides have similar inhibitory potency. These results have implications for the known role of diacylglycerol kinase ε in neuronal function and in epilepsy since the action of this enzyme will remove 1-stearoyl-2-arachidonoylglycerol, the precursor of the endocannabinoid 2-arachidonoyl glycerol.