Dietary intervention and simvastatin is beneficial in the prevention cardiovascular diseases by lowering plasma lipid levels. Endothelial dysfunction is associated with coronary artery disease and its risk factors and is reversed by dietary intervention. It has been suggested that hyperlipidemia con...
Dietary intervention and simvastatin is beneficial in the prevention cardiovascular diseases by lowering plasma lipid levels. Endothelial dysfunction is associated with coronary artery disease and its risk factors and is reversed by dietary intervention. It has been suggested that hyperlipidemia contributes to the development of atherosclerosis by increasing inducible nitric oxide synthase (iNOS) expression via intimal thickening. Statins treatment has been found to decrease iNOS expression and atherogenensis in animal models. We hypothesized that dietary intervention and simvastatin therapy could decrease plasma nitric oxide in hypercholesterolemic patients, which would suggest the opportunity for modulation of iNOS expression through the use of statins in a clinical situation. We measured the plasma levels of nitrite and nitrate (NOx) in 19 hyperlipidemia patients. The subjects were under dietary intervention following simvastatin therapy for 12 weeks. As a result, the plasma level of NOx, stable metabolites of nitric oxide (NO), saw a two-fold elevation in hyperlipidemic patients as compared to normal levels. Although 12 weeks of dietary intervention did not lower NOx levels, subsequent 12-week simvastatin (10 mg/day) treatment, along with dietary intervention, lowered NOx levels significantly. This NOx reduction, induced by simvastatin therapy, positively correlated with lowered coronary risk factors (r=0.40, p=0.02). It indicated that simvastatin therapy decreases plasma NOx levels by, perhaps, decreasing iNOS expression or activity leading to the attenuation of the development of neointima.
Dietary intervention and simvastatin is beneficial in the prevention cardiovascular diseases by lowering plasma lipid levels. Endothelial dysfunction is associated with coronary artery disease and its risk factors and is reversed by dietary intervention. It has been suggested that hyperlipidemia contributes to the development of atherosclerosis by increasing inducible nitric oxide synthase (iNOS) expression via intimal thickening. Statins treatment has been found to decrease iNOS expression and atherogenensis in animal models. We hypothesized that dietary intervention and simvastatin therapy could decrease plasma nitric oxide in hypercholesterolemic patients, which would suggest the opportunity for modulation of iNOS expression through the use of statins in a clinical situation. We measured the plasma levels of nitrite and nitrate (NOx) in 19 hyperlipidemia patients. The subjects were under dietary intervention following simvastatin therapy for 12 weeks. As a result, the plasma level of NOx, stable metabolites of nitric oxide (NO), saw a two-fold elevation in hyperlipidemic patients as compared to normal levels. Although 12 weeks of dietary intervention did not lower NOx levels, subsequent 12-week simvastatin (10 mg/day) treatment, along with dietary intervention, lowered NOx levels significantly. This NOx reduction, induced by simvastatin therapy, positively correlated with lowered coronary risk factors (r=0.40, p=0.02). It indicated that simvastatin therapy decreases plasma NOx levels by, perhaps, decreasing iNOS expression or activity leading to the attenuation of the development of neointima.
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가설 설정
The n-3 faty acids promote the synthesis of the beneficial nitric oxide in the endothelium. In this study, we demonstrated that dietary intervention had no effect on plasma nitric oxide levels. The ineffectiveness of the dietary intervention may have been due to the limited changes in energy intake and cholesterol intake without an n-3 ratio change.
제안 방법
The objective of the study was to clarify the effect of dietary intervention and simvastatin therapy on plasma NO concentration in hyperlipidemia, the lipid profile and coronary risk factors.
diet. The patients moved from a basal diet containing 19% fat (182.7 mg cholesterol/day), 16% protein and 84% carbohydrate to a diet containing 18% fat (139.2 mg cholesterol/day), 16% protein, and 65% carbohydrate for 12 weeks.
대상 데이터
The subjects were 19 hyperlipidemic patients (4 males and 15 females) whose plasma triglyceride and total cholesterol levels were 그200 mg/dL, as measured at the Medical Examination Center of K university. Mean age of the 19 hyperlipidemic subjects was 58.
Simvastatin therapy and dietary intervention were conducted according to the Korean guidelines for the treatment of hyperlipidemic patients. Thirty-six normal subjects were selected from among medical school students at I university, whose plasma triglyceride and total cholesterol level동 were < 200 mg/dL.
데이터처리
Results are expressed as mean+SE. Two-way ANOVA with repeated measures was used to compare simvastatin and placebo treatments. When a significant difference was revealed using this analysis, comparisons at each drug infusion level were made using two-tailed t tests.
Two-way ANOVA with repeated measures was used to compare simvastatin and placebo treatments. When a significant difference was revealed using this analysis, comparisons at each drug infusion level were made using two-tailed t tests. A value of p<0.
이론/모형
The dietary intervention involved the substitution of v/hite meat and fish for fatty and red-meat products; increasing the consumption of vegetables, legumes and fmit; reducing egg consumption; and avoiding sweets and pastries. Nutrition intake was determined, before and after the 12-week dietary intervention, using the 24 hr recall method. The records of foods eaten were assessed through personal interviews at two-week interv이s.
Plasma levels of lipids (triglycerides, cholesterol, HDL-cholesterol) were quantified using the enzymatic method on Reflotron system automated analyzers (Boehringer Manheim). Plasma levels of LDL cholesterol were calculated using Fredewald's formula. Apolipoprotein A-l and apolipoprotein B were determined using immunonephelometry on a Kallestad QM 300 system.
(24th week) simvastatin therapy. Plasma levels of lipids (triglycerides, cholesterol, HDL-cholesterol) were quantified using the enzymatic method on Reflotron system automated analyzers (Boehringer Manheim). Plasma levels of LDL cholesterol were calculated using Fredewald's formula.
성능/효과
The results also showed that 12 weeks of simvastatin therapy decreased plasma levels of TC, LDL-C and apo B, all significantly, without affecting the TG level. Conversely, the plasma levels of HDL-C and apo A-l increased significantly.
후속연구
1). Though further research is necessary, this result may be explained by the expression of iNOS, which is known to produce large amounts of NO continuously, in human atherosclerotic lesions. While it was not possible to assess the extent of atherosclerotic lesions present in our patients, this increased plasma NOx may have originated from the infiltrated macrophages or vascular smooth muscle cells expressing iNOS at many unkown sites.
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