BackgroundHyperhomocysteinemia (HHcy) causes increased oxidative stress and is an independent risk factor for cardiovascular disease. Oxidative stress is now believed to be a major contributory factor in the development of non alcoholic fatty liver disease, the most common liver disorder worldwide. In this study, the changes which occur in homocysteine (Hcy) metabolism in high fat-diet induced non alcoholic fatty liver disease (NAFLD) in rats were investigated.Methods and resultsAfter feeding rats a standard low fat diet (control) or a high fat diet (57% metabolisable energy as fat) for 18 weeks, the concentration of homocysteine in the plasma was significantly raised while that of cysteine was lowered in the high fat as compared to the control diet fed animals. The hepatic activities of cystathionine β-synthase (CBS) and cystathionine γ-lyase (CGS), the enzymes responsible for the breakdown of homocysteine to cysteine via the transsulphuration pathway in the liver, were also significantly reduced in the high fat-fed group.ConclusionsThese results indicate that high fat diet-induced NAFLD in rats is associated with increased plasma Hcy levels caused by down-regulation of hepatic CBS and CGL activity. Thus, HHcy occurs at an early stage in high fat diet-induced NAFLD and is likely to contribute to the increased risk of cardiovascular disease associated with the condition.
Hyperlipidaemia, atherosclerosis and related diseases are becoming a major health problem in developing countries. Ocimum basilicum is one of the medicinal plants widely used in Morocco to reduce plasma cholesterol and to reduce the risk of atherosclerosis-related diseases. However, mechanisms underlying the reported hypolipidaemic effect of this plant have not been investigated. This study evaluates the lipid lowering effect of aqueous Ocimum basilicum extract in Triton WR-1339-induced hyperlipidaemic rats. Hyperlipidaemia was developed in animals by intraperitoneal injection of Triton (200 mg/kg). After injection of Triton the animals were divided into three treatment groups: hyperlipidaemic, hyperlipidaemic plus herb extract and hyperlipidaemic plus fenofibrate treated rats. At 7 h after the Triton injection, levels of plasma cholesterol, triglycerides and LDL-cholesterol in rats treated also with the Ocimum basilicum extract (0.5 g/100 g body weight) were, respectively, 50%, 83% and 79% lower than Triton-treated rats and HDL-cholesterol was 129% higher than in rats given Triton alone. At 24 h following Ocimum basilicum administration, total cholesterol, triglycerides and LDL-cholesterol levels decreased by 56%, 63% and 68%, respectively, in comparison with the Triton treated group and HDL-cholesterol was not increased significantly. The hypolipidaemic effect exerted by Ocimum basilicum extract was markedly stronger than the effect induced by fenofibrate treatments. Further it was demonstrated that Ocimum basilicum aqueous extract displayed a very high antioxidant power. These results indicate that Ocimum basilicum extract may contain hypolipidaemic and antioxidant substances and its use as a therapeutic tool in hyperlipidaemic subjects may be of benefit and encourage further investigation in this field.
The effects of chylomicron remnants on lipid accumulation in J774 macrophages, and the incorporation of radioactivity from remnant lipids radiolabelled with [3H]oleate into cellular lipids was investigated. After 24 h of incubation with chylomicron remnants, there was considerable accumulation of lipid within the cells as assessed by staining with oil red O, indicating that the particles induce the formation of foam cells. Fatty acids released from the radiolabelled remnant lipids after uptake were found to be incorporated into cellular triacylglycerol (52%), phospholipid (37%) and cholesteryl ester (8%), but at higher remnant concentrations, the proportion used for triacylglycerol formation increased (up to 73%). When the macrophages were shifted into a pro-oxidising or pro-reducing state by incubation (24 h) with CuSO4 (2.5 µM) or N-acetylcysteine (5 mM), respectively, the incorporation of [3H]oleate from remnant lipid into cellular triacylglycerol and phospholipid was increased by 20–30% in the more oxidised as compared with the more reduced cells. These findings indicate that exposure of J774 macrophages to chylomicron remnants leads to the accumulation of lipid within the cells, and that this process is enhanced by pro-oxidising conditions. We conclude, therefore, that both lipids of dietary origin and the redox balance within macrophages may have a significant role in the induction of foam cell formation.
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