Palm Tocotrienols Protect Against Diet-Induced Atheroma Formation

The formation of the atherosclerotic plaque is not simply the accumulation of cholesterol and cholesterol esters within arterial walls. Instead, it's a complex dynamic process, involving several key players or factors. For example, the arterial endothelium releases ‘chemotaxis factors' which attract monocytes from the circulation into the sub-endothelial space, the oxidation of low density lipoproteins (LDLs) and the recognition of these oxidised forms by phagocytes, the coagulant activity of the thrombogenic 'villain' factor VII, the release of platelet-derived growth factor (PDGF), and the migration of smooth muscle cells. Finally, calcification sets in hardening the lesion and the rest is bad news!

We know that palm tocotrienols have a statinlike cholesterol-lowering action by suppressing 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase activity, the rate-limiting enzyme in hepatic cholesterol biosynthesis. We also know that these Vitamin E species can inhibit LDL oxditation, but to what extent do such antioxidant properties actually prevent atheroma formation?

A recent study conducted by researchers from the University of North Carolina at Chapel Hill helped provide answers in this regard. In their study, apoB-deficient mice were fed a non-purified control diet, an atherogenic diet alone, or atherogenic diet supplemented with specific amounts of palm Vitamin E (0.5 or 1.5g/100g), alpha-tocopherol (0.5/100g), or palm carotenoids (0.01 g/100 g) for a period of 3 months.

The mice used in the study were deficient in apoE (high affinity ligand for the LDL receptor) which meant defective clearance of chylomicra and very low density lipoprotein (VLDL) remnants from the circulation. Thus, when provided with an atherogenic diet, plasma TC would rise a few folds, excess cholesterol accumulate in the liver, and atheromas form in these animals.

The palm Vitamin E supplements, but not the alpha-tocopherol nor beta-carotene supplements, reduced dramatically the above adverse effects obtained with the atherogenic diet. For example, the 1.5g/100g palm Vitamin E supplement reduced plasma TC by 60%, while both concentrations of palm Vitamin E supplements reduced the size of the atheromas by half, compared with animals on the atherogenic diet alone.

Two observations were particularly thought-provoking. One is that the plasma lipid values of the animals fed the lower 0.5g/100g palm Vitamin E supplement were largely unchanged and yet the size of the atheromas were reduced by the half. What this means is that reduction of lesion formation in these diets must have occurred by mechanisms other than cholesterol control alone.

The second is that the statin-like effect of tocotrienols was probably not in operation in the dietary atherogenic model used and yet the 1.5g/100g palm Vitamin E supplement was able to decrease hepatic cholesterol concentration and to normalise plasma lipoproteins. Suggested possible mechanisms operating are independent of antioxidant action such as increased hepatic bile synthesis and secretion, as well as reduced intestinal cholesterol absorption.

Source :
Nutrition Briefs January 2002.
Published by Malaysian Palm Oil Promotion Council, Kuala Lumpur, Malaysia.

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