Diet is the first (and sometimes the only) therapeutic approach to hyperlipoproteinaemias. Rice bran oil and its main components (unsaturated fatty acids, triterpene alcohols, phytosterols, tocotrienols, alpha-tocopherol) have demonstrated an ability to improve the plasma lipid pattern of rodents, rabbits, non-human primates and humans, reducing total plasma cholesterol and triglyceride concentration and increasing the high density lipoprotein cholesterol level. Other potential properties of rice bran oil and gamma-oryzanol, studied both in vitro and in animal models, include modulation of pituitary secretion, inhibition of gastric acid secretion, antioxidant action and inhibition of platelet aggregation. This paper reviews the available data on the pharmacology and toxicology of rice bran oil and its main components with particular attention to those studies relating to plasma lipid altering effects.
Monthly Archives: June 2001
Synergistic effect of tocotrienol-rich fraction (TRF(25)) of rice bran and lovastatin on lipid parameters in hypercholesterolemic humans
Qureshi AA, Sami SA, Salser WA, Khan FA
J Nutr Biochem. 2001 Jun;12(6):318-329.
Tocotrienols exert hypocholesterolemic action in humans and animals. Lovastatin is widely used for that purpose. Both agents work by suppressing the activity of beta-hydroxy-beta-methylglutaryl coenzyme A reductase through different mechanisms, post-transcriptional vs competitive inhibition. A human study with 28 hypercholesterolemic subjects was carried out in 5 phases of 35 days each, to check the efficacy of tocotrienol-rich fraction (TRF(25)) of rice bran alone and in combination with lovastatin. After placing subjects on the American Heart Association (AHA) Step-1 diet (phase II), the subjects were divided into two groups, A and B. The AHA Step-1 diet was continued in combination with other treatments during phases III to V. Group A subjects were given 10 mg lovastatin, 10 mg lovastatin plus 50 mg TRF(25), 10 mg lovastatin plus 50 mg alpha-tocopherol per day, in the third, fourth, and fifth phases, respectively. Group B subjects were treated exactly to the same protocol except that in the third phase, they were given 50 mg TRF(25) instead of lovastatin.The TRF(25) or lovastatin plus AHA Step-1 diet effectively lower serum total cholesterol (14%, 13%) and LDL-cholesterol (18%, 15% P < 0.001), respectively, in hypercholesterolemic subjects. The combination of TRF(25) and lovastatin plus AHA Step-1 diet significantly reduces of these lipid parameters of 20% and 25% (P < 0.001) in these subjects. Substitution of TRF(25) with alpha-tocopherol produces insignificant changes when given with lovastatin. Especially significant is the increase in the HDL/LDL ratio to 46% in group (A) and 53% (P < 0.002) in group (B). These results are consistent with the synergistic effect of these two agents. None of the subjects reported any side-effects throughout the study of 25-weeks. In the present study, the increased effectiveness of low doses of tocotrienols (TRF(25)) as hypocholesterolemic agents might be due to a minimum conversion to alpha-tocopherol. The report also describes in vivo the conversion of gamma-[4-3H]-, and [14C]-desmethyl (d-P(21)-T3) tocotrienols to alpha-tocopherol.
This study investigated the effects of a tocotrienol-rich fraction (TTRF) on the microscopic development of atherosclerosis and lipid peroxidation in the aorta of rabbits. Group 1 was fed a normal diet, group 2 received a 2% cholesterol diet and group 3 received a 2% cholesterol diet plus daily oral administration of the TTRF. After 10 weeks, the aortic content of malondialdehyde (MDA) was measured as an index of lipid peroxidation. The MDA was lowest in rabbits that received the TTRF compared to the groups that did not. The degree of intimal thickening was higher in the cholesterol-fed rabbits without the TTRF compared to the cholesterol-fed rabbits with TTRF (P<0.05). The continuity of the internal elastic lamina (IEL) was noted to be preserved in the cholesterol-fed rabbits with TTRF but appeared disrupted in the cholesterol-fed rabbits without the TTRF. The disrupted and fragmented IEL may have resulted from the injury caused by lipid peroxidation that contributed to the more extensive intimal thickening. We conclude that the antioxidant activities of the TTRF can reduce experimental atherosclerosis.