6-ketoprostaglandin-f1-alpha and eicosapentaenoic-acid-ethyl-ester

Wistar rats (4-week-old) were administered with streptozotocin (45 mg/kg) through tail veins. After 3 months, diabetic rats were divided into 2 groups. One group (EPA group, n = 16) was fed a lipid-free diet (90%, w/w) plus lard (8%) and 90% pure eicosapentaenoic acid ethyl ester (2%) for 6 months. The other group (control group, n = 16) was fed in the same way except that eicosapentaenoic acid ethyl ester was replaced by safflower oil. Twenty-four-hour urine was collected just before starting the experimental diets and during the 6-month experimental period at monthly intervals. There were no differences in food intake and body weight between the two groups throughout the experiment. The mean microalbuminuria of the EPA group became significantly lower than that of the control group after 4 months on the diets through the end of the study (6 months). The mean microalbuminuria levels at the end of the study were 1.38 mg/day in the EPA group (n = 9) and 5.19 mg/day in the control group (n = 6) (p < 0.01). Eicosapentaenoic acid administration might retard the progression of diabetic nephropathy by reducing microalbuminuria.

Topics: 6-Ketoprostaglandin F1 alpha; Albuminuria; Animals; Blood Glucose; Blood Pressure; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Eating; Eicosapentaenoic Acid; Fatty Acids; Kidney; Lipids; Male; Organ Size; Rats; Rats, Wistar; Thromboxane B2; Weight Gain

A highly purified ethyl ester of EPA (EPAEE) (74%) was manufactured from sardine oil. Sixty mg/kg/day of EPAEE was given orally to male Wistar rats for 8 weeks. No side effect or toxicity from the administration of EPAEE was observed. Plasma EPA concentration and the ratio of EPA to arachidonic acid were significantly increased, compared with control Wistar rats. An enhancement of PGI2-like substance production by aortas obtained from rats fed EPAEE was noted. Conversion of EPA to delta 17-6-keto-PGF1 alpha, a stable metabolite of PGI3, could not be detected by an incubation study of 14C-EPA and aortas either from rats fed EPAEE or from control rats. Therefore, PGI2-like substance produced by rat aorta is most likely to be PGI2 itself and not PGI3.

Topics: 6-Ketoprostaglandin F1 alpha; Administration, Oral; Animals; Aorta, Thoracic; Arachidonic Acid; Arachidonic Acids; Eicosapentaenoic Acid; Epoprostenol; Fatty Acids; Fatty Acids, Unsaturated; Lipids; Male; Platelet Aggregation; Prostaglandins; Rats; Rats, Inbred Strains