• Journal of Nutrition and Health
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• v.26 no.7
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• pp.819-828
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• 1993

The reaction of lecithin cholesterol acyltransferase(LCAT) and cholesteryl ester transfer protein (CETP) are important in cholesterol esterification and transfer for the reverse cholesterol transport(RCT) system. The purpose of this study were to assess the effects of fatty acid unsaturation on RCT system. After 12 female human subjects consumed a prescribed high saturated fat diet prior to the period, two groups of six subjects were provided with a high PUFA(corn oil) or a high SFA(butter) as major fats in a 40 en % fat diet. Butter feeding increased plasma total-(34%), esterified-(96%), HDL_3$-(23%), LDL-(20%), and VLDL plus LDL(35%) cholesterol while corn oil feeding decreased esterified-(25%), LDL(15%) cholesterol and TG(27%). There were significant differences of fats on total-(p=0.0001), esterified-(p=0.0001), total HDL-(p=0.005), $HDL_2$-(p=0.01)and LDL-(p=0.0001) cholesterol. LCAT activity did not change during the period but highly correlated to apo A-I in HDL which was increased in the corn oil group. The 2.5 fold increased CETP activity in the butter group during the period might be related to changes in plasma VLDL plus LDL cholesterol level which were increased in the butter group.

• Journal of Nutrition and Health
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• v.31 no.8
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• pp.1235-1243
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• 1998

Although an elevated plasma level of high density lipoprotein (HDL) is known as a protective component against the development of atherosclerosis and ensuing coronary heart diseases, the related mechanisms are still not established . It has been clearly demonstrated in the early stages of atherogenesis that adhesion of monocytes and lymphocytes to the vascular endothelium is enhanced via adhesion molecules, and that monocytes and macrophages accumulate in the subendothelial space. The present study has investigated whether isolated plasma HDL plays a role in protection against atherogenesis by inhibiting the expression of vascular cell adhesioin molecule-1(VCAM-1) on the endothelial cells. Effects of plasma native low density lipoprotein (LDL) and ac ethylated LDL(AcLDL) on VCAM-1 expression were also examined by using an immunocytochemical technique. While plasma HDL did not alter the basal expression of VCAM-1 , lipopolysaccharide(LPS) induction of this adhesion modlecule was markedly inhibited at a phyaiological concentration of HDL. In contrast, 30$\mu\textrm{g}$ protein/ml AcLDL increased sifnificantly both basal VCAM-1 expression and its LPD induction , suggesting that this modified LDL enhances leukocyte adhesiion to endothelial cells. Unlike AcLDL , plasma native LDL inhibited significantly VCAM-1 expression. This indicates that LDL did not undergo oxidative modificantion while incubated with endothelial cells. These results suggest that plasam HDL may inhibit atherogenesis by reducing the expression of adhesion molecules, which is a protective mechanism independent of tis reverse cholesterol transport function . Modified LDL is a potent iducer for adhesion molecules in vascular endothelical cells and could play a role in the pathogenesis of atherosclerosis by adhering to blood cells.

• Preventive Nutrition and Food Science
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• v.7 no.4
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• pp.454-460
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• 2002

While atherosclerosis is a major killer, there is now concern that mortality from the disease will increase due to the rising incidence of type II diabetes. Because diet can potentially influence both diseases, it is important to elucidate the role of diet in the progression of atherosclerosis. In addition, the mechanisms involved in dietary-related alterations of the disease need to be defined to guide public health recommendations to reduce athero-sclerosis incidence and limiting unwanted side effects. Since diet is thought to play a role in atherosclerosis even without added complications due to type II diabetes, reducing the incidence of that metabolic disease will not be enough. While evidence is increasing that high intake of carbohydrate can lead to type II diabetes and atherosclerosis, the preponderance of existing evidence indicates that intake of specific fats as a major dietary causal factor. It has recently been hypothesized that a dietary fat link to atherosclerosis may depend partly on the activity of a transcriptional regulator, the peroxisome proliferator activated receptors (PPAR). Thusfar, PPAR $\alpha$, $\beta$/$\delta$ and ${\gamma}$, have been shown to play a major role in metabolism, inflammation, and cancer. Furthermore, PPAR may regulate specific processes associated with atherosclerosis such as triglyceride and low density lipoprotein (LDL) metabolism; the reverse cholesterol transport pathway; lipid accumulation within plaques; the local inflammatory response and plaque stability. Synthetic ligands for PPAR have been developed; however, natural ligands include specific fatty acids and their metabolites. Though the role of PPAR in atherosclerosis has been reported with respect to synthetic ligands, additional studies need to be done with established and possible natural ligands. In this review, we will focus on the relation of dietary fat to PPAR alteration of atherosclerosis.