Diglyceride
Adiglyceride,ordiacylglycerol(DAG), is aglycerideconsisting of twofatty acidchainscovalently bondedto aglycerolmolecule throughesterlinkages.[1]Two possible forms exist, 1,2-diacylglycerols and 1,3-diacylglycerols. Diglycerides are natural components of food fats, though minor in comparison totriglycerides.[2]DAGs can act assurfactantsand are commonly used asemulsifiersin processed foods.DAG-enriched oil(particularly 1,3-DAG) has been investigated extensively as afat substitutedue to its ability to suppress the accumulation of body fat;[3][4]with total annual sales of approximately USD 200 million in Japan since its introduction in the late 1990s till 2009.[3]
Production[edit]
Diglycerides are a minor component of manyseed oilsand are normally present at ~1–6%; or in the case ofcottonseed oilas much as 10%.[5]Industrial production is primarily achieved by aglycerolysisreaction betweentriglyceridesand glycerol. The raw materials for this may be eithervegetable oilsoranimal fats.[6]
Food additive[edit]
Diglycerides, generally in a mix withmonoglycerides(E471), are common food additives largely used asemulsifiers.The values given in the nutritional labels for total fat, saturated fat, andtransfat do not include those present in mono- and diglycerides.[citation needed]They often are included in bakery products, beverages,ice cream,peanut butter,chewing gum,shortening,whipped toppings,margarine,confections, and some snack products, such asPringles.
Biological functions[edit]
Protein kinase C activation[edit]
In biochemical signaling, diacylglycerol functions as asecond messengersignaling lipid,and is a product of thehydrolysisof the phospholipidphosphatidylinositol 4,5-bisphosphate(PIP2) by the enzymephospholipase C(PLC) (amembrane-bound enzyme) that, through the same reaction, producesinositol trisphosphate(IP3). Although inositol trisphosphate diffuses into thecytosol,diacylglycerol remains within theplasma membrane,due to itshydrophobicproperties. IP3stimulates the release of calcium ions from the smoothendoplasmic reticulum,whereas DAG is a physiological activator ofprotein kinase C(PKC). The production of DAG in the membrane facilitates translocation of PKC from the cytosol to theplasma membrane.
Munc13 activation[edit]
Diacylglycerol has been shown to exert some of its excitatory actions on vesicle release through interactions with the presynaptic priming protein familyMunc13.Binding of DAG to the C1 domain of Munc13 increases the fusion competence of synaptic vesicles resulting in potentiated release.
Diacylglycerol can be mimicked by the tumor-promoting compoundsphorbol esters.[7]
Other[edit]
In addition to activating PKC, diacylglycerol has a number of other functions in thecell:
- a source forprostaglandins
- a precursor of theendocannabinoid2-arachidonoylglycerol
- an activator of a subfamily oftransient receptor potential canonical(TRPC) cation channels, TRPC3/6/7.
Metabolism[edit]
Synthesis of diacylglycerol begins withglycerol-3-phosphate,which is derived primarily fromdihydroxyacetone phosphate,a product ofglycolysis(usually in the cytoplasm of liver or adipose tissue cells). Glycerol-3-phosphate is firstacylatedwith acyl-coenzyme A (acyl-CoA) to formlysophosphatidic acid,which is then acylated with another molecule of acyl-CoA to yieldphosphatidic acid.Phosphatidic acid is then de-phosphorylated to form diacylglycerol.
Dietary fat is mainly composed oftriglycerides.Because triglycerides cannot be absorbed by the digestive system, triglycerides must first be enzymatically digested intomonoacylglycerol,diacylglycerol, or free fatty acids. Diacylglycerol is a precursor totriacylglycerol(triglyceride), which is formed in the addition of a third fatty acid to the diacylglycerol under the catalysis ofdiglyceride acyltransferase.
Since diacylglycerol is synthesized via phosphatidic acid, it will usually contain a saturated fatty acid at the C-1 position on the glycerol moiety and an unsaturated fatty acid at the C-2 position.[8]
Diacylglycerol can be phosphorylated to phosphatidic acid bydiacylglycerol kinase.
Insulin resistance[edit]
Activation ofPKC-θby diacylglycerol may causeinsulin resistancein muscle by decreasingIRS1-associatedPI3Kactivity.[9]Similarly, activation ofPKCεby diacyglycerol may cause insulin resistance in the liver.[9][10]
See also[edit]
References[edit]
- ^IUPAC,Compendium of Chemical Terminology,2nd ed. (the "Gold Book" ) (1997). Online corrected version: (2006–) "glycerides".doi:10.1351/goldbook.G02647
- ^"Toxicological evaluation of some food additives including anticaking agents, antimicrobials, antioxidants, emulsifiers and thickening agents".World Health Organization.
- ^abPhuah, Eng-Tong; Tang, Teck-Kim; Lee, Yee-Ying; et al. (2015)."Review on the Current State of Diacylglycerol Production Using Enzymatic Approach"(PDF).Food and Bioprocess Technology.8(6): 1169–1186.doi:10.1007/s11947-015-1505-0.ISSN1935-5130.S2CID84353775.
- ^Lo, Seong-Koon; Tan, Chin-Ping; Long, Kamariah; et al. (2008)."Diacylglycerol Oil—Properties, Processes and Products: A Review"(PDF).Food and Bioprocess Technology.1(3): 223–233.doi:10.1007/s11947-007-0049-3.ISSN1935-5130.S2CID86604260.
- ^Flickinger, Brent D.; Matsuo, Noboru (February 2003). "Nutritional characteristics of DAG oil".Lipids.38(2): 129–132.doi:10.1007/s11745-003-1042-8.PMID12733744.S2CID4061326.
- ^Sonntag, Norman O. V. (1982). "Glycerolysis of fats and methyl esters — Status, review and critique".Journal of the American Oil Chemists' Society.59(10): 795A–802A.doi:10.1007/BF02634442.ISSN0003-021X.S2CID84808531.
- ^Blumberg, Peter M. (1988)."Protein Kinase C as the Receptor for the Phorbol Ester Tumor Promoters: Sixth Rhoads Memorial Award Lecture".Cancer Research.48(1): 1–8.PMID3275491.
- ^Berg J, Tymoczko JL, Stryer L (2006).Biochemistry(6th ed.). San Francisco: W. H. Freeman.ISBN0-7167-8724-5.[page needed]
- ^abErion DM, Shulman GI (2010)."Diacylglycerol-mediated insulin resistance".Nature Medicine.16(4): 400–402.doi:10.1038/nm0410-400.PMC3730126.PMID20376053.
- ^Petersen MC, Madiraju AK, Gassaway BM, et al. (2016)."Insulin receptor Thr1160 phosphorylation mediates lipid-induced hepatic insulin resistance".Journal of Clinical Investigation.126(11): 4361–4371.doi:10.1172/JCI86013.PMC5096902.PMID27760050.