Influence of ω-3 fatty acid treatment on cardiac phospholipid composition and coronary flow of streptozocin-diabetic rats

Abstract

Cardiac effects of ω-3 fatty acid treatment were studied in streptozocin (STZ)-induced (55 mg/kg intravenously [IV]) diabetic male Wistar rats. Nondiabetic control and STZ-diabetic animals were treated with Promega (0.5 mL/kg/d; Warner-Lambert, Morris Plains, NJ) for a period of 4 weeks beginning 2 weeks after either vehicle or STZ injection. Plasma glucose, triglyceride, and cholesterol concentrations were significantly ( P < .05) elevated in diabetic animals; ω-3 fatty acid treatment did not significantly affect these parameters. An isolated working heart preparation was used to determine aortic and coronary flow rates in control, diabetic, treated control, and treated diabetic animals. Aortic and coronary flow rates of untreated STZ-diabetic rats were significantly ( P < .05) lower than those of controls over a range of left atrial filling pressures (7.5 to 20 cm water). Both aortic and coronary flow rates of ω-3 fatty acid-treated diabetic animals were significantly ( P < .05) increased above those of untreated diabetic rats. Aortic and coronary flow rates of treated diabetic rats paralleled those of control animal; ω-3 fatty acid treatment did not affect aortic or coronary flow rates of control animals. Cardiac phosphatidylcholine (PC) and phosphatidylethanolamine (PE) and sarcoplasmic reticulum (SR) total phospholipid were isolated and the acyl composition was determined. Stearic acid and C22:4, n-6 were significantly reduced in cardiac PE of diabetic animals. Relative to PE acyl species of untreated nondiabetic controls, treated diabetic PE had increased eicosapentaenoic acid (EPA) and decosahexaenoic acid (DHA) and reduced C22:4, n-6 levels. Compared with respective untreated groups, there was a significant increase in the amount of PE EPA in ω-3 fatty acid-treated control and diabetic animals. Alterations in acyl content of PC were restricted to ω-3 fatty acid-treated controls; compared with untreated controls, reductions in C18:2, n-6 and C22:4, n-6 and an increase in EPA levels were found. EPA, which is not detectable in cardiac SR of untreated animals, accounted for 1.6% and 0.7% of the total acyl species of treated control and treated diabetic animals, respectively. DHA levels increased by 22% and 16% to account for 14.3% and 16.6% of ω-3 fatty acid-treated control and diabetic SR acyl species, respectively. The changes in SR DHA content were not significant. These data suggest that mechanisms in addition to membrane phospholipid alterations may be responsible for the ω-3 fatty acid-mediated effect on aortic and coronary flow in STZ-diabetic rats.