title: Dietary n-3 fatty acids alter angiotensin-induced contraction and 1,2-diacylglycerol fatty acid composition in thoracic aortas from diabetic rats.
abstract: The effect of diabetes on the incorporation of long-chain n-3 fatty acids into thoracic aorta smooth muscle phospholipids and 1,2-diacylglycerol, and on the contractile response of aortic rings to angiotensin II, was examined in streptozotocin-induced diabetic rats. In diabetic animals fed a diet containing 1% of fatty acids as n-3 fatty acids, smooth muscle membrane levels of 18:2n-6 were elevated in phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol, whereas 20:4n-6 was depleted. The resultant decreased ratios of 20:3/18:2 and 20:4/20:3 indicate inhibition of delta6- and delta5-desaturase activity in the diabetic state. A diet containing 5% of fatty acids as n-3 fatty acids increased phospholipid levels of eicospentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) several-fold, but with a further reduction in 20:4n-6. Similarly, 1,2-diacylglycerol from rats fed the high n-3 diet was enriched in EPA, DPA and DHA. When incubated with 10(-8) M angiotensin II, the contractile response of intact aortic rings from diabetic animals fed the high n-3 diet was only 60.8+/-9.3% that of controls fed the same diet. However, contractile response was not significantly different from control animals fed the low n-3 diet (55.6+/-7.9%). The results indicate that vascular smooth muscle phospholipid n-6 and n-3 fatty acid metabolism is altered in diabetes, resulting in changes to the fatty acid profile of 1,2-diacylglycerol. Moreover, elevating membrane phospholipid and 1,2-diacylglycerol content of EPA, DPA and DHA partially ameliorates the depressed response to angiotensin II seen in the diabetic state.
authors.affiliation: Department of Oral Health Sciences, University of Alberta, Edmonton, Canada. dpehowic@gpu.srv.ualberta.ca
authors.forename: D J
authors.initials: DJ
authors.lastname: Pehowich
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000737:chemistry* / Q000187:drug effects / Q000502:physiology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D004042:Dietary Fats, Unsaturated / Q000494:pharmacology*; D004075:Diglycerides / Q000737:chemistry; D004305:Dose-Response Relationship, Drug; D005227:Fatty Acids / Q000032:analysis / Q000737:chemistry*; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects* / Q000502:physiology; D010713:Phosphatidylcholines / Q000737:chemistry; D010714:Phosphatidylethanolamines / Q000737:chemistry; D010716:Phosphatidylinositols / Q000737:chemistry; D051381:Rats; D017207:Rats, Sprague-Dawley; D014886:Weaning
chemical_list: D004042:Dietary Fats, Unsaturated; D004075:Diglycerides; D005227:Fatty Acids; D015525:Fatty Acids, Omega-3; D010713:Phosphatidylcholines; D010714:Phosphatidylethanolamines; D010716:Phosphatidylinositols; D000804:Angiotensin II