Dietary modification of fatty acid and prostaglandin synthesis in the rat. Effect of variations in the level of dietary fat.
Dietary supplements with safflower oil, linseed oil, cod liver oil and hydrogenated coconut oil were given to rats at levels of 5, 20 and 40 energy % to simultaneously assess the effects of both type and level of dietary fat on tissue fatty acid composition and prostanoid synthesis. There was no significant change in weight gain or blood pressure between the dietary groups after the 4-week dietary regimen. The liver oil and linseed oil diets depressed the arachidonic acid content of kidney phospholipids at all levels of supplementation. The arachidonic acid content of plasma lipids was significantly elevated in animals on the safflower oil diet at 20 and 40 energy % while those on the same level of liver oil diet showed a marked reduction in arachidonic acid. Whole blood synthesis of thromboxane B2 varied significantly at all levels of fat supplementation, with the 20 energy % safflower oil fed group showing maximally enhanced thromboxane B2 production compared to the coconut oil group (P less than 0.001). Conversely, the liver oil groups showed depressed thromboxane B2 synthesis at 20 and 40 energy % (P less than 0.01) compared to the coconut oil group and at 5 energy % compared to the safflower oil group (P less than 0.05). Production of 6-ketoprostaglandin F1 alpha and prostaglandin E2 by incubated kidney homogenates only differed significantly between the dietary groups at 40 energy %. Urinary excretion of 6-ketoprostaglandin F1 alpha was increased by 45% and 55% in rats fed the safflower oil diet at 20 and 40 energy %, respectively compared to the saturated fat diet, while in the liver oil groups excretion was reduced by 20% and 32%. Dietary suppression of prostanoid synthesis is explained in part by changes in available arachidonic acid and competitive inhibition of cyclooxygenase by (n - 3) fatty acids. Thus, minor changes in dietary fat can readily alter tissue fatty acid composition, but both the extent and nature of changes in phospholipid and prostanoid metabolism vary markedly according to the tissue site.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D004041:Dietary Fats / Q000494:pharmacology*; D005227:Fatty Acids / Q000096:biosynthesis* / Q000097:blood; D007668:Kidney / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D009821:Oils; D010743:Phospholipids / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis* / Q000652:urine; D051381:Rats; D011919:Rats, Inbred Strains; D013329:Structure-Activity Relationship; D013929:Thromboxane B2 / Q000097:blood
D004041:Dietary Fats; D005227:Fatty Acids; D009821:Oils; D010743:Phospholipids; D011453:Prostaglandins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha