Abstract
The content and molecular species composition of 1,2-diacylglycerol (DAG) in rat sciatic nerve was determined and compared with the molecular species profiles for glycerophospholipid classes in order to gain information concerning the metabolic pathways of DAG formation. The level of DAG in freshly dissected epineurium-free nerve (44±2 pmol/mg wet weight) was 10-40% of that in other tissues and cultured cells. The predominant DAG molecular species were 18: 0/20: 4 (30%) and 16: 0/18: 1 (17%). In comparison with phospholipid molecular species patterns, DAG was characterized by a substantial but lower proportion of the 18: 0/20: 4 species than was found in phosphoinositides, and a significant fraction of saturated species such as those found in phosphatidylcholine. In nerve from diabetic rats, both the content and arachidonoyl-containing molecular species of DAG were reduced. These species were also decreased in individual glycerophospholipids, except for phosphatidylinositol. The distribution of molecular species in phosphatidc acid (PA) did not resemble that of any other phospholipid. A large rise in DAG content occurred when nerve was incubated in vitro.Molecular species analysis indicated that phosphoinositides were the main source, especially during the initial period. This process was virtually abolished in a Ca2+-free medium and probably reflects a response to tissue injury. Evidence was obtained for the isomerization of DAG to 1,3-diacylglycerol during incubation. PA content and molecular species composition of incubated nerve did not change. However, inclusion of propranolol, a PA phosphatase inhibitor, caused a 40% accumulation of PA within 10 min, suggesting that formation of this phospholipid is continuous. These findings support the conclusion that DAG is principally derived from phosphoinositides by phospholipase C hydrolysis, but a minor fraction could be derived from phosphatidylcholine either by the action of phospholipase C or via phospholipase D and PA phosphatase. The metabolic origins of PA appear to be diverse.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Billah MM and Anthes JC (1990) The regulation and cellular functions of phosphatidylcholine hydrolysis. Biochem J 269: 281–291.
Cameron NE, Cotter MA, Robertson S (1991) Essential fatty acid supplementation: Effects on peripheral nerve and skeletal muscle function and capillarization in streptozocin-induced diabetic rats. Diabetes 40: 532–539.
de Chaffoy de Courcelles D, Roevens P, Van Beller H, Kennis L, Somers Y, De Clerck F (1989) The role of endogenously formed diacylglycerol in the propagation and termination of platelet activation. J Biol Chem 264: 3274–3285.
Dang AQ, Kemp K, Faas FH, Carter WJ (1989) Effects of dietary fats on fatty acid composition and Δ5 desaturase in normal and diabetic rats. Lipids 24: 882–889.
Day NS, Berti-Mattera LN, Eichberg J (1991) Muscarinic cholinergic receptormediated phosphoinositide metabolism in rat sciatic nerve. J Neurochem 56: 1905–1913.
Dennis EA, Rhee SG, Billah MM, Hannun YA (1991) Role of phospholipases in generating lipid second messengers in signal transduction. FASEB J 5: 2068–2077.
Eck MG, Wynn JO, Carter WJ, Faas FH (1979) Fatty acid desaturation in experimental diabetes mellitus. Diabetes 28: 479–485.
Ehle H, Mueller E, Horn A (1985) Alkaline phosphatase of calf intestine hydrolyzes phospholipids. FEBS Lett 183: 413–416.
Exton JH (1990) Signaling through phosphatidylcholine breakdown. J Biol Chem 265: 1–4.
Holman RT, Johnson SB, Gerrard JM, Mauer SM, Kupcho-Sandberg S, Brown DM (1983) Arachidonic acid deficiency in streptozotocin-induced diabetes. Proc Nat Acad Sci USA 80: 2375–2379.
Holub BJ, Kuksis A, Thompson W (1970) Molecular species of mono-di-and triphosphoinositides of bovine brain. J Lipid Res 11: 558–564.
Jamal GA and Carmichael H (1990) The effect of gamma-linolenic acid on human diabetic neuropathy: A double-blind placebo-controlled trial. Diabetic Med 7: 319–323.
Julu POO (1988) Essential fatty acids prevent slowed nerve conduction in streptozotocin diabetic rats. J Diabetic Complications 2: 185–188.
Kennerly DA (1987) Diacylglycerol metabolism in mast cells. J Biol Chem 262: 16305–16313.
Kodali DR, Tercyak A, Fahey DA, Small DM (1990) Acyl migration in 1,2-dipalmitoyl-sn-glycerol. Chem Phys Lipids 52: 163–170.
Lattimer SA, Sima AAF, Greene DA (1989) In vivo correction of Na+,K+-ATPase activity in diabetic nerve by protein kinase C agonists. Am J Physiol 256: E264–E269.
Lee C and Hajra AK (1991) Molecular species of diacylglycerols and phosphoglycerides and the postmortem changes in the molecular species of diacylglycerols in rat brains. J Neurochem 56: 370–379.
Lin C-J, Peterson RG, Eichberg J (1985) The fatty acid composition of glycerolipids in nerve, brain and other tissues of the streptozotocin diabetic rat. Neurochem Res 10: 1453–1465.
Loffelholz K (1989) Receptor regulation of choline phospholipid hydrolysis. Biochem Pharmacol 38: 1543–1549.
Mavis RD, Bell RM, Vagelos PR (1972) Effect of phospholipase C hydrolysis of membrane phospholipids on membranous enzymes. J Biol Chem 247: 2835–2841.
Pappu AS and Hauser G (1983) Propranolol-induced inhibition of rat brain cytosolic phosphatidate phosphohydrolase. Neurochem Res 8: 1565–1575.
Pessin MS and Raben DM (1989) Molecular species of 1,2-diglyceride stimulated by α-thrombin in culture fibroblasts. J Biol Chem 264: 8729–8738.
Poisson JP (1985) Comparative in vivo and in vitro study of the influence of experimental diabetes on rat liver linoleic acid Δ6 and Δ5 desaturation. Enzyme 34: 1–4.
Preiss J, Loomis CR, Bishop WR, Stein R, Niedel JE, Bell RM (1986) Quantitative measurement of sn-l,2-diacylglycerols present in platelets, hepatocytes and rasand sis-transformed normal rat kidney cells. J Biol Chem 258: 764–769.
Rana RS and Hokin LE (1990) Role of phosphoinositides in transmembrane signaling. Physiol Rev 70: 115–163.
Serdarevich B (1967) Glyceride isomerization in lipid chemistry. J Am Oil Chem Soc 44: 381–393.
Simmons DA and Winegrad AI (1991) Elevated extracellular glucose inhibits an adenosine-(Na+, K+)-ATPase regulatory system in rabbit aortic wall. Diabetologia 34: 157–163.
Sunako M, Kawahara Y, Hirata K, Tsuda T, Yokoyama M, Fukazaki H, Takai Y (1990) Mass analysis of 1,2-diacylglycerol in cultured rabbit vascular smooth muscle cells. Hypertension 15: 84–88.
Sutherland CA and Amin D (1982) Relative activities of rat and dog platelet phospholipase A2 and diglyceride lipase: Selective inhibition of diglyceride lipase by RHC80267. J Biol Chem 257: 14006–14010.
Tomlinson DR, Robinson JP, Compton AM, Keen P (1989) Essential fatty acid treatment: Effects on nerve conduction, polyol pathway and axonal transport in streptozotocin diabetic rats. Diabetologia 32: 655–659.
Wright TM, Rangan LA, Shin HS, Raben DM (1988) Kinetic analysis of 1,2-diacylglycerol mass levels in cultured fibroblasts. J Biol Chem 263: 9374–9380.
Yao JK, Dyck PJ, VanLoon JA, Mover TP (1981) Free fatty acid composition of human and rat peripheral nerve. J Neurochem 36: 1211–1218.
Zhu X and Eichberg J (1990a) 1,2-Diacylglycerol content and its arachodonylcontaining molecular species are reduced in sciatic nerve from streptozotocininduced diabetic rats. J Neurochem 55: 1087–1090.
Zhu X and Eichberg J (1990b) A pool of myo-inositol needed for phosphatidylinositol synthesis is depleted in diabetic nerve. Proc Nat Acad Sci USA 87: 9818–9822.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1992 Springer Science+Business Media New York
About this chapter
Cite this chapter
Eichberg, J., Zhu, X. (1992). Diacylglycerol Composition and Metabolism in Peripheral Nerve. In: Bazan, N.G., Murphy, M.G., Toffano, G. (eds) Neurobiology of Essential Fatty Acids. Advances in Experimental Medicine and Biology, vol 318. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3426-6_37
Download citation
DOI: https://doi.org/10.1007/978-1-4615-3426-6_37
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-6515-0
Online ISBN: 978-1-4615-3426-6
eBook Packages: Springer Book Archive