Cereal grains, alpha tocotrienol and cholesterol metabolism in the rat.

The influence of alpha (α)-tocotrienol, the main vitamer of vitamin E in barley and oats, on cholesterol synthesis has been studied in laboratory rats. Both oats and barley lowered plasma cholesterol relative lo wheat, which had no such effect, and the change has been attributed to an inhibitory influence of a -tocotrienol on cholesterol synthesis rate. Vitamin E was stripped from oats and barley by a petroleum ether extraction procedure and the grains compared with their unstripped equivalents. In the oats feeding experiment this resulted in a higher plasma cholesterol and lower liver cholesterol synthesis rate. The barley experiment produced no significant response. Pure α-tocotrienol was gavaged into rats fed a semipurified diet without vitamin E, at the rate of 380 µg/rat/day for 28 days. There was no significant influence on plasma cholesterol level or on liver cholesterol synthesis rate. From these studies it is concluded that a -tocotrienol does not influence cholesterol synthesis rate significantly. Therefore, it is unlikely lo be a factor in oats and barley responsible for the plasma cholesterol lowering observed.

The influence of linoleate and vitamin E from sunflower seed oil on platelet function and prostaglandin production in the common marmoset monkey.

Vitamin E and linoleate, both of which are found in high concentrations in sunflower seed oil, were examined independently for their influence on general and blood-vascular parameters in vitamin E-deficient common marmosets. A vitamin E-deficient diet (-E, 4 micrograms/g) was supplemented with either 40 micrograms/g vitamin E (+E), vitamin E stripped sunflower oil (+10% SSO-E), or SSO (+10% SSO w/w) in a 2 x 2 factorial designed experiment, and the diets fed for 9 months to 4 even groups of common marmosets. Vitamin E deficiency was associated in marmosets with a loss of skeletal muscle mass and of body weight, enhanced peroxidative haemolysis of erythrocytes, increased white blood cell counts, and in the SSO-E group a relative neutrophilia. Platelet reactivity was increased with vitamin E deficiency, and to a greater degree with the SSO-E group. Aortic prostacyclin production was significantly increased by the addition of vitamin E, linoleate and both as SSO to the deficient diet, the effects being additive. Fatty acid changes associated with the different treatments reflected the influence of high linoleate and vitamin E treatments. The platelet and aortic arachidonate value in the SSO-E group showed the lowest and most variable value, and this was associated with greatest platelet aggregability. An adequate vitamin E intake is essential for stabilising high PUFA diets and biomembranes and enhancing the protective role of prostacyclin in blood vessels against thrombogenesis.

Influence of dietary fats on blood coagulation and prostaglandin production in the common marmoset.

Common marmosets were fed a standard marmoset diet (REF) or diets supplemented with 12% (wt/wt) sunflower seed oil (SSO) or sheep fat (SF) for a period of 90 weeks. The values for coagulation indices, clotting time, and Russel viper venom time were consistent with decreased thrombotic tendency of platelets from animals on the SSO diet relative to the low fat, REF diet animals, while an increased tendency to thrombosis was observed with SF-fed marmosets. The SSO- and SF-supplemented marmosets showed a significantly reduced thromboxane (TXB2) generation from platelets aggregating to collagen (ASC) relative to the REF group, while at 50 micrograms/ml ASC this difference was maintained only by the SSO group. The SF diet-fed marmosets showed a reduced prostacyclin (measured as 6-keto-PGF1 alpha) generation from incubated aorta relative to the REF or SSO-fed groups, which were not different from each other. A reduced proportion of platelet phospholipid arachidonic acid (20:4, n-6) and increased alpha-tocopherol concentration was consistent with the decreased aggregability and thromboxane generation of platelets from SSO-fed marmosets relative to the REF and SF groups. The SF diet-fed marmosets, on the other hand, showed minimal change in arachidonic acid, alpha-tocopherol or platelet reactivity from the REF group. These differing responses to dietary fats are discussed in relation to the potential for the development of thrombosis and atherosclerosis.

The influence of dietary fats on plasma lipids, blood pressure and coagulation indices in the rat.

Male Hooded Wistar rats were fed a commercial rat diet supplemented 12% by weight with sheep fat, sunflower seed oil and fish oil (tuna) over a period of 8 months. The influence of these diets on plasma fatty acids, triglycerides and cholesterol, blood pressure, body weight and coagulation indices was assessed. The sheep fat (SF)-fed rats showed a significant increase in body weight over the reference group (C) of 18%, and systolic blood pressure increased by 9.4%, whereas other dietary groups were not significantly affected. The fish oil (TFO)-fed rats showed a significant lowering of plasma cholesterol (-16.6%) and triglyceride (-47%) relative to the reference group, while the sunflower seed oil (SSO) group showed only a lowered plasma triglyceride (-32%). Plasma fatty acids in general reflected closely the dietary fatty acids, with some exceptions. Coagulation indices provided a consistent picture of an increased tendency to thrombosis in SF-fed rats and a significantly reduced tendency in the TFO-fed rats relative to reference rats. Fish oil rich in 20:5 and 22:6 omega 3 long-chain polyunsaturated fatty acids and low in cholesterol appears to have advantages in terms of reducing those parameters identified as risk factors for coronary heart disease in man. Sheep fat supplements rich in saturated fatty acids produce the opposite trend.

Experimental oxalate urolith formation in rats.

Urinary calculi composed of calcium oxalate were produced in male hooded Wistar rats fed a vitamin B6 deficient diet over 16 weeks. This basic diet was modified by doubling the phosphate content or loading with vitamin C or D3 in three treatment groups. The number of rats developing oxalate stones was not altered by the addition of vitamin D3 or phosphate, but there was a significant increase in total weight of stone formed and histological evidence of extensive renal damage in rats on the high vitamin D3 diet. The addition of vitamin C to the vitamin B6 deficient rats resulted in a reduction in the number of rats with uroliths and a fall in urinary oxalate excretion, while similarly loaded vitamin B6 supplemented controls were free of oxalate calculi. It is concluded that the oxalate urolithiasis induced by vitamin B6 deficiency was exacerbated by added vitamin D3 and reduced by vitamin C.