Serum HDL-C XAV939 levels were significantly higher in the hypercholesterolaemic hamsters compared to those on the normal diet. This observation is in agreement with previous studies in humans and hamsters where KU-0059436 high-cholesterol diet caused HDL-C elevation. In addition, the increased HDL-C levels in cholesterol-fed hamsters could also be an adaptive mechanism showing the need to enhance cholesterol efflux through the reverse cholesterol transport pathway in response to the high-cholesterol diet. The metabolism of LDL-C is greatly influenced by the number and activity of LDL receptors. Hence, functional LDL receptors are vital to take up LDL-C in order to decrease their circulating levels in the blood circulation which is one of the contributing factors towards the development of atherosclerosis. The effect of the plant extract on the expression of LDL receptor gene was studied to ascertain if the cholesterol-lowering effect of the plant extract occurred through increased production of LDL receptors. In the present study, the gene expression of LDL receptor in T. indica fruit pulp-fed hamsters was not significantly different from control hamsters. Similarly, the serum concentration of LDLC in both groups of animals was not significantly different. The expression of LDL receptor in hamsters fed on the high-cholesterol diet was significantly down-regulated, signifying the possibility that high intracellular cholesterol reduced and suppressed synthesis of LDL receptors. LDL-C in excess was not efficiently taken up by the limited amounts of LDL receptors, hence decreasing LDL-C clearance from peripheral tissues. This could explain the elevation of serum LDL-C observed in the present study. Another gene that was measured in this study was Apo A1 which codes for Apolipoprotein A1. Apo A1 is one of the major lipoprotein constituents of HDL-C and is involved in cholesterol efflux from tissues to liver for excretion. Some studies have reported inverse relationship between serum Apo A1 levels and CHD. Similarly, over-expression of Apo A1 in Apo A1 transgenic mice has been shown to increase HDL-C and reduce the risk against diet-induced atherosclerosis. The possible mechanism exerted by Apo A1 to provide cardioprotective effects include its role in reversing cholesterol transport which is the main pathway to eliminate excess cholesterol from peripheral tissues and to transport them to the liver. Cholesterol in the liver is then partially converted into bile acids and subsequently excreted in bile. Thus, the concentration of HDL-C is highly correlated with Apo A1 levels and Apo A1 gene expression may be an essential determinant of HDL-C. Therefore, increasing the production of Apo A1 by enhancing its gene transcription in the liver would be greatly advantageous. In this study, hepatic expression of Apo A1 was down-regulated in hamsters fed with high-cholesterol diet compared with control, indicating that the cholesterol-enriched diet suppressed the Apo A1 expression which could have led to the observed elevated total cholesterol and triglyceride levels. A report showed that highcholesterol diet decreased the levels of Apo A1 in rabbits. However, in this study, the down-regulation of Apo A1 expression was not accompanied by a decreased in HDL-C levels in the hypercholesterolaemic hamsters. This is unexpected because suppression of Apo A1 gene is predicted to also decrease HDL-C levels. It is possible that other mechanisms maybe involved in regulating HDL-C levels. For instance, overexpression of lecithin cholesterol acyltransferase in hamsters had been reported to increase HDL-C levels. T. indica fruit pulp supplementation to normal hamsters neither altered the expression of hepatic Apo A1 gene nor the levels of HDL-C.