蝇蛆壳聚糖降血脂作用的实验研究

目的探讨蝇蛆壳聚糖降血脂的作用。方法预防性给药时，给高脂饲料造模的同时连续给药4w，于第28天测定大鼠血清TC、TG、HDL-C、LDL-C含量，同时观察对大鼠体重、肝重及肝重/体重百分率的影响。治疗性给药时，给高脂饲料造模成功后连续给药4w，测定大鼠血清TC、TG、HDL-C、LDL-C含量，并观察对大鼠体重、肝重及肝重/体重百分率的影响。结果预防性给药时，中、高剂量蝇蛆壳聚糖组能显著降低血清TC、TG、LDL-C含量，显著升高HDL-C，降低大鼠体重、肝重及肝重/体重百分率。治疗性给药时，低、高剂量蝇蛆壳聚糖组能显著降低血清TC、TG、LDL-C含量，显著升高HDL-C，降低大鼠体重、肝重及肝重/体重百分率。结论蝇蛆壳聚糖能调节血脂平衡，预防高脂血症的产生，对已形成的高脂血症有一定的治疗效果。     

虎杖降脂颗粒对高脂血症大鼠降脂作用的研究

目的研究虎杖降脂颗粒对饮食性大鼠高脂血症的治疗作用。方法采用高脂性饮食诱导大鼠高脂血症,给予口服不同剂量的虎杖降脂颗粒,观察药物对模型动物血脂水平、体质量变化和肝脏脏器指数,肝脏脂质TC、TG,血清AST、ALT、肌酐和尿素氮以及肝脏组织形态的影响。结果虎杖降脂颗粒各剂量组大鼠肝指数及肝组织脂质TC和TG均明显下降(P0.05或P0.01);血清中TC、LDL-C、HDL-C含量不同程度地降低(P0.05或P0.01),但对TG作用不明显;血清AST、ALT有不同程度的降低(P0.05或P0.01),但对血清肌酐和尿素氮无明显作用。肝组织病理学结果表明,虎杖降脂颗粒各剂量组能不同程度地降低模型大鼠的肝脏脂肪变性程度。结论虎杖降脂颗粒可有效调节高脂乳剂所致高脂血症大鼠血脂和肝脂水平,对高脂血症具有较好的调脂作用。     

姜黄素固体分散体对大鼠血脂水平的影响

目的 探讨姜黄素固体分散体对大鼠血脂及抗氧化能力的影响.方法 采用喷雾干燥法制备姜黄素固体分散体;以雄性SD大鼠为实验对象,高脂乳剂造模,同时灌胃给予姜黄素、固体分散体,测定大鼠血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)含量,同时测定血清和肝匀浆中的超氧化物岐化酶(SOD)活性、丙二醛(MDA)含量.结果 姜黄素固体分散体与姜黄素比较能显著地降低高脂模型大鼠血清TC、TG、LDL-C含量(P＜0.01);升高血清HDL-C含量(P＜0.01);提高血清及肝匀浆的SOD活性;降低MDA含量.结论 喷雾干燥法制备的姜黄素固体分散体对实验性高脂血症大鼠有良好的降脂及抗氧化作用.     

益气活血法抗实验性高脂血症大鼠脂质过氧化机制的研究

目的探讨益气活血法抗实验性高脂血症大鼠脂质过氧化机制。方法采用高脂高胆固醇法,复制大鼠高脂血症病理模型。观察比较给药组与病理模型组的总胆固醇(TC)、三酰甘油(TG)、一氧化氮(NO)及肝中丙二醛(MDA)的水平。结果补肾益气活血药小剂量组血清TC、TG、低密度脂蛋白(LDL-C)明显低于模型组。同时显著升高高密度脂蛋白(HDL-C),明显降低动脉硬化指数(P<0.001)。补肾益气活血药大剂量组抑制高脂血症大鼠肝脏脂质过氧化,其肝中MDA含量较模型组明显下降(P<0.05或P<0.01),NO水平较模型组明显升高(P<0.05或P<0.01)。结论补肾益气活血为主的中药复方可调整和改善血瘀痰浊范围内的高脂血症引起的高粘、高浓、高凝、高聚状态,其作用机制与抑制氧自由基,脂质过氧化有关。     

北五味子多糖对高脂血症大鼠肝损伤的影响

目的探讨北五味子多糖(SCP)对高脂饮食诱导肝损伤大鼠肝功能的保护作用。方法采用高脂饲料喂养16 w诱发高脂血症大鼠模型,随机分为模型组及SCP治疗组,另设正常对照组以及正常+SCP组。SCP(50 mg/kg)灌胃给药12 w,检测各组动物血清中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,肝组织中TG和TC水平;苏木素-伊红(HE)染色观察药物对肝组织病理学改变的影响。结果与正常对照组比较,模型组大鼠血清中TC、TG、LDL-C、ALT及AST水平显著增高(P<0.01),肝组织中TG和TC水平显著增高(P<0.01)。与模型组比较,SCP显著降低了大鼠血清TC、TG、LDL-C水平(P<0.05或P<0.01)、ALT、AST水平(P<0.01),降低肝组织中TG和TC水平(P<0.01),而对正常大鼠血脂、肝脂质和肝功能没有明显影响。HE染色显示模型组大鼠肝小叶结构紊乱,出现明显的肝细胞脂肪变性;SCP组肝小叶结构基本正常,肝脏脂肪变性明显减轻。结论 SCP可改善高脂血症大鼠脂质代谢紊乱,改善肝功能,减轻肝损伤。     

保肝降脂饮对脂肪肝大鼠护肝作用的实验研究

目的探讨保肝降脂饮治疗脂肪肝的药学机制。方法采用高脂饮食诱导大鼠脂肪肝模型,实验分组为脂肪肝模型组、保肝降脂饮大、中、小剂量组、东宝肝泰对照组和正常对照组共6组。观察大、中、小剂量保肝降脂饮和东宝肝泰对大鼠血清中胆固醇(TC)、甘油三酯(TG)的含量和肝组织的超氧化物歧化酶(SOD)活性的影响,以及肝组织形态学的变化。结果模型组大鼠血清中TC、TG明显高于正常组和各治疗组(P<005),而其SOD的活性较正常组和各治疗组明显降低。肝组织切片脂滴明显堆积,正常组没有脂滴堆积,各治疗组肝组织切片显示脂滴堆积较模型组轻。结论保肝降脂饮可显著降低脂肪肝大鼠血清TC、TG含量,减轻肝细胞脂滴堆积,提高肝组织SOD活性,从而发挥降脂保肝的作用。     

氟伐他汀钠对大鼠高脂血症模型的实验研究

目的 探讨氟伐他汀钠(来适可)对高脂血症老龄大鼠血脂的影响.方法 选择健康Wister大鼠随机分为4组,采用高脂血症模型,用酶法检测血清中胆固醇(TC)、三酰甘油(TG)含量,化学修饰法检测血清中低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)的指标.结果 来适可和利之舒均能降低血清中TC、TG、LDL-C含量,升高HDL-C(P<0.05).结论 动物实验研究发现,来适可具有调脂作用.     

大豆肽对实验性高脂血症大鼠血脂的影响及其机制

目的研究大豆肽对实验性高脂血症模型大鼠血脂代谢的影响并探讨其降脂机制。方法建立高脂血症大鼠模型,将45只Wistar大鼠随机分为5组,即正常组+正常饲料、高脂模型组+高脂饲料、大豆肽低、中、高剂量组+添加相应剂量大豆肽的高脂饲料,喂饲40 d后检测相关指标。结果与高脂模型组相比,大豆肽中、高剂量组的血清总胆固醇(TC)、甘油三酯(TG)含量显著降低(P<0.05),高密度脂蛋白(HDL-C)含量升高但无显著性差异(P>0.05),大鼠总脂酶(PHTA)、肝脂酶(HL)和脂蛋白脂酶(LPL)活性明显增强(P<0.05)。结论大豆肽能有效降低实验性高脂血症大鼠血脂水平,其降脂作用可能与提高血清中PHTA、HL和LPL活性有关。     

华夏小葱制剂对脂肪肝大鼠脂质代谢和组织形态学的影响

目的:观察华夏小葱制剂对脂肪肝大鼠防治作用及其对组织形态学影响.方法:60只SD大鼠随机分为空白对照组(n= 10),模型对照组(n=10),华夏小葱制剂低剂量组(n=10),中剂量组(n=10),高剂量组(n =10)以及东宝肝泰片组(n=10)。空白对照组用普通饲料及普通水喂养;其他组用高脂饮食及酒精水喂养,并结合每周一次行后肢sc小剂量四氯化碳色拉油溶液的方法建立大鼠脂肪肝模型.用光镜及电镜观察肝脏的形态学改变情况,采用全自动生化分析仪测定总胆固醇(TC),甘油三酯(TG),低密度脂蛋白胆固醇fLDL-C),高密度脂蛋白胆固醇(HDL-C),ALT(丙氨酸氨基转移酶),AST(天门冬酸氨基转移酶),TP(总蛋白),ALB(清蛋白)、GLO(球蛋白)及A/G(清蛋白/球蛋白)的含量.结果:光镜和电镜观察均见模型对照组有严重脂肪变性,脂滴增多;华夏小葱低、中、高剂量组及东宝肝泰片组脂肪变性程度有所减轻,脂滴不同程度的有所减少.和空白对照组的TC,TG,HDL-C,LDL-C,ALT,AST,TP,ALB相比,模型对照组大鼠血浆TC,TG,LDL-C,ALY,AST值均显著升高(P<0.01),HDL-C,TP,ALB值均显著降低(P<0.01);和模型对照组的TC,TG,HDL-C,LDL-C,ALT,AST TP,ALB相比,华夏小葱低,中,高剂量组及东宝肝泰片组TC,TG,LDL-C值均显著降低(TC:低,中,高剂量组P<0.05,东方肝泰片组P<0.01;TG:低,中剂量组和东方肝泰片平P<0.05,高剂量细P<0.01:LDL-C:均P<0.05),HDL-C值与模型对照组相比显著升高(均P<0.05),ALY,AST值与模型对照组相比无统计学差异,华夏小葱高剂量组与模型对照组相比ALB值显著升高(P<0.05).结论:华夏小葱制剂能改善脂肪肝大鼠体内的脂质代谢,对脂肪肝有一定的防治作用.     

玉米黄素对实验性高脂血症小鼠血脂的影响

目的 探讨玉米黄素对实验性高脂血症小鼠血脂的调节作用.方法 健康昆明种小鼠50只,雌雄各半,按体重随机分为5组:正常对照组;高脂模型组;玉米黄素低、中、高剂量组 (20、40、60 mg/kg).正常对照组喂基础饲料,其余各组喂高脂饲料,自由饮水;正常对照组和高脂模型组灌胃蒸馏水,其余各组灌胃相应剂量的玉米黄素.4 w后,断头取血,用试剂盒测定血清甘油三酯( TG)、总胆固醇( TC)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)含量.结果 与正常对照组比较,高脂模型组血清TC 、TG、LDL-C水平升高具有统计学意义(P<0.01);与高脂模型组比较,玉米黄素低、中、高剂量组血清TC、LDL-C水平降低具有显著性差异(P<0.01),且玉米黄素高剂量组血清TG水平下降也有统计学意义(P<0.05).结论 玉米黄素对实验性高脂小鼠具有调节血脂的作用.     

Tamoxifen therapy and hepatic steatosis

Tamoxifen has been used for a long time as a hormonal treatment in breast cancer. Recent studies in pre and postmenopausal women have shown that tamoxifen exhibits favorable effects on the lipid profile. In this study we investigated the effects of tamoxifen on lipid profile and hepatic steatosis. Fifty two (31 postmenopausal and 21 premenopausal) women with breast cancer treated with tamoxifen at a dose of 20 mg daily were included in the study. Serum lipid parameters (total cholesterol, high and low density lipoprotein cholesterol and triglyceride) were measured baseline and at the 6th month of tamoxifen treatment. Upper abdominal ultrasonography was performed before and at the 6th month of therapy for assessment of liver steatosis. We obtained decreased levels of serum total cholesterol after 6 months of tamoxifen treatment (p < 0.05). However, we did not detect any changes in triglyceride and high-density lipoprotein cholesterol levels (p > 0.05). Increased liver steatosis was observed in 22 patients (42.3%) after tamoxifen treatment. We could not detect increase in lipid levels in these patients. There was no significant difference between the lipid levels in the patients with increased liver steatosis and stable or no liver steatosis. Whether hepatic steatosis is dependent on lipid changes in tamoxifen use should be further investigated.     

Effect of long-term clofibric acid treatment on serum and tissue lipid and cholesterol levels in obese Zucker rats

The long-term effects of clofibric acid (200 mg/kg body weight) injected subcutaneously from 6-36 weeks of age were assessed in obese, hyperlipemic Zucker rats. At 18 and 36 weeks of age, treated rats had significantly lower fasted serum cholesterol levels but triacylglycerol levels were not affected. Rats were killed at 36 weeks of age at which time there were no differences in body and kidney weights between control and clofibric acid-treated rats. Liver, spleen and heart weights were lowered by clofibric acid treatment. In liver there was an elevation of lipid/g due to treatment but there were no effects on cholesterol/g or on either total liver lipid or cholesterol levels. In the epididymal fat pad of clofibric acid-treated rats, there was a 21% elevation of cholesterol level on a per pad basis. In the other organs, there were no effects of treatment on lipid or cholesterol levels except for lowered total cholesterol in kidney. Several liver lipogenic enzymes were lowered by treatment but malic enzyme was two times higher.     

Sterol carrier protein 2 gene transfer changes lipid metabolism and enterohepatic sterol circulation in mice

BACKGROUND & AIMS: Sterol carrier protein 2 (SCP-2) enhances sterol cycling and facilitates cholesterol translocation between intracellular organelles and plasma membrane in cultured cells, including hepatocytes. We examined the role of SCP-2 in hepatic cholesterol and lipid trafficking through the sinusoidal and canalicular secretory pathways of the liver in vivo. METHODS: Recombinant adenovirus-mediated SCP-2 gene transfer was used to obtain hepatic overexpression of SCP-2 in C57BL/6 mice. RESULTS: SCP-2 overexpression in the mouse liver resulted in an 8-fold increase of SCP-2 protein levels and determined various effects on lipid metabolism. It decreased high-density lipoprotein cholesterol and increased low-density lipoprotein (LDL) cholesterol concentrations. The expressions of hepatic LDL receptor, apolipoprotein (apo) A-I, apoB, and apoE were decreased. SCP-2 overexpression also increased hepatic cholesterol concentration, associated with decreased cholesterol neosynthesis. Increased biliary cholesterol and bile acid secretion, bile acid pool size, and intestinal cholesterol absorption were also observed. CONCLUSIONS: These results indicate that modulation of SCP-2 expression in the liver determines important modifications on lipoprotein metabolism, hepatic cholesterol synthesis and storage, biliary lipid secretion, bile acid metabolism, and intestinal cholesterol absorption.     

Effects of dietary protein and fiber on growth and selected cholesterol responses of rats

The effect of dietary protein and fiber on growth and metabolic parameters in blood serum, liver and kidney were determined in a 2 X 5 factorial experiment involving 40 Sprague-Dawley rats. Treatment variables were two dietary protein levels (16 and 24%) and five acid detergent fiber levels (6, 10, 16, 24 and 34%). No difference in growth rate of rats was found due to varying levels of either protein or fiber in the diet. Increasing the dietary protein level from 16 to 24% resulted in an 18.5% reduction in blood cholesterol. The dietary treatment containing 16% fiber influenced most metabolic parameters examined, including blood serum cholesterol, liver cholesterol and total lipid content in liver and kidney. Rats receiving the diet containing 16% fiber had the highest serum cholesterol (88.9 mg/dl) and the lowest liver cholesterol (4.4 mg/g) as compared with other fiber groups.     

Circulating lipoproteins and hepatic sterol metabolism in Psammomys obesus prone to obesity, hyperglycemia and hyperinsulinemia.

The liver plays a central role in lipoprotein metabolism and cholesterol homeostasis. As the physiopathology of lipid disorders in non-insulin-dependent diabetes mellitus (NIDDM) is multifactorial and still imperfectly known, we evaluated its onset on plasma lipid transport and hepatic cholesterol metabolism in Psammomys obesus. This sand rat lapses into hyperinsulinemia and hyperglycemia when transferred from its native food to laboratory rodent diets. Marked hypertriglyceridemia and hypercholesterolemia developed in hyperinsulinemic (Group B) and hyperglycemic/ hyperinsulinemic (Group C), compared with normal P. obesus (Group A). Group B showed significantly (P<0.05) higher plasma VLDL-cholesterol (41.9%) and LDL-cholesterol (47.3%) concentrations, whereas Group C was characterized by an even more marked increase in VLDL-cholesterol (176%, P<0.001) compared with Group A. Lipoprotein composition was also altered, displaying impaired lipid and apolipoprotein moiety distribution in IDL, LDL, HDL(2) and HDL(3) lipoprotein fractions of Groups B and C. The activity of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol biosynthesis, was consistently lower in Group B (P<63.4%, P<0.001) and C (43.9%, P<0.005). In contrast, the direct measurement of microsomal acyl-CoA:cholesterol acyltransferase (ACAT), controlling the acylation of cholesterol, showed an increase averaging 53% in Group B (P<0.01) and 61% in Group C (P<0.005). Similarly, elevated activity (171.1%, P<0.05 and 291.4%, P<0.001, respectively) was related to cholesterol 7alpha-hydroxylase, the rate-limiting enzyme in bile acid biosynthesis. These alterations were accompanied with abundant deposition of triglycerides and cholesterol in the liver. Changes in circulating lipids and liver parameters were related to glucose and insulin levels, indicating the implication of insulin resistance and diabetes. Therefore, our findings demonstrate various disturbances in plasma lipid profile and lipoprotein composition, as well as in liver cholesterol metabolism during the sequential development of insulin resistance and diabetes in P. obesus rats. Furthermore, the current data point to an undoubtedly important role of the liver in the pathogenesis of metabolic disorders in the progression of nutritionally-induced insulin resistance and diabetes in P. obesus. Finally, current research shows that more marked plasma and hepatic lipid perturbations occur in insulin resistance than in diabetes, which may culminate in the development of atherosclerosis.     

Actions of vitamins A and E and some nicotinic acid derivatives on plasma lipids and on lipid infiltration of aorta in cholesterol-fed rabbits.

Marked hypercholesterolemia and moderate lipid infiltration of the aorta were induced by feeding rabbits a diet containing 1% cholesterol + 3% corn oil for 70 days. In the liver the concentration and pool size of cholesterol increased and those of triglycerides (TG) decreased. On dietary addition of vitamin A and vitamin E (44 000 I.U. and 125 mg respectively, once daily for 5 days a week) the following changes were noted in comparison with the fat-fed rabbits not receiving extra addition of vitamins. There was a slight decrease of the levels of plasma cholesterol and an increase of those of plasma TG. The liver cholesterol concentration increased but, according to the concomitant reduction of the liver weight, there was no significant change in lever cholesterol or TG pools. In the aorta the vitamins markedly reduced the lipid infiltrated area as well as the cholesterol content. Both niceritrol** and S-2040 [pyridine-2,5-dicarboxylic acid di(beta-pyridylcarbinol ester)] in a dietary concentration of 0.5% decreased plasma cholesterol by about 20%. This reduction, as well as that induced by the vitamins, was confined to the VLDL-fractions only. S-2040 slightly reduced the cholesterol accumulation in the aorta. In rabbits given both the vitamins and niceritrol or S-2042 there was an additive reduction of plasma cholesterol. Here the nicotinic acid derivatives were partly able to counteract the increases of plasma TG induced by the vitamins. In the aorta the combination vitamins + S-2042 but not that of vitamins + niceritrol tended to give a better protection than the vitamins alone. On a normal diet vitamins A + E significantly increased the liver cholesterol concentration and pool and decreased the liver TG pool, but did not affect the other parameters. Possible mechanisms for the prophylactic action of the vitamins against lipid infiltration of the aorta of cholesterol-fed rabbits are discussed.     

Effect of pollen extract on the development of experimental atherosclerosis in rabbits

Our previous studies have shown that the pollen extract, Cernitin, reveals lipid-lowering properties in animals and humans. The present study was designed to investigate the influence of Cernitin on the development of experimental atherosclerosis in rabbits over a period of 12 weeks. Forty male mongrel rabbits were divided into 4 equal groups: (1) controls, (2) animals receiving high-fat diet (HFD) containing cholesterol and coconut oil, (3) HFD + pollen extract, and (4) HFD + clofibrate. The most pronounced reduction in lipid metabolism and in the severity of plaque formation occurred after the pollen extract had been applied. The total cholesterol content in serum and liver homogenate was depressed by 67% and 45%, respectively, while the serum HDL cholesterol and alpha-lipoproteins level was increased by 19% and from 7.73% to 21.73% respectively. The cytochrome P-450 content in the liver microsomes was elevated by 98% (nmol/g liver). Atherosclerotic plaque intensity at 12 weeks, measured planimetrically, averaged 85.5% in HFD-fed animals vs 33.7% in pollen extract-treated rabbits. These findings suggest that Cernitin, in addition to significantly lowering serum lipid levels in rabbits on an experimental diet, may modify lipid deposition in major arteries.     

炎症干扰胆固醇调节元件结合蛋白2致ApoE/SRA/CD36三基因敲除小鼠肝脏脂质的异常积聚

目的 研究炎症是否通过干扰核转录因子胆固醇调节元件结合蛋白2(SREBP-2)而致ApoE/SRA/CD36三基因敲除小鼠肝脏胆固醇的异常积聚.方法 将8周龄ApoE/SRA/CD36三基因敲除雄性小鼠随机分为对照组(n=8)和炎症组(n=8),2组均喂以西方饮食(Western diet),炎症组小鼠皮下注射10%酪蛋白建立慢性炎症模型,对照组注射相应量磷酸盐缓冲液,14周后处死,测定血清中炎症介质和脂质的水平及肝组织中胆固醇含量,油红O、免疫组织化学染色后观察肝脂质沉积程度以及组织形态变化,实时定量PCR法检测肝脏SREBP裂解激活蛋白(SCAP)、SREBP-2及其下游基因低密度脂蛋白受体(LDLr)mRNA水平.对计量资料采用两样本均数比较的t检验进行统计学分析.结果 炎症状态下,血清中总胆固醇[(7.72±1.70)mmol/L]、低密度脂蛋白胆固醇[(2.94±0.44)mmol/L]、高密度脂蛋白胆固醇[(2.24±0.63)mmol/L]水平均显著降低,与对照组[分别为(13.23±3.61)mmol/L、(9.28±3.66)mmol/L、(4.13±0.42)mmol/L]比较,t值分别为3.383、4.245、5.937,P值均＜0.05;肝组织中胆固醇含量显著增加;油红O染色表明,胆固醇在肝脏中的沉积异常增多(t=2.707,P＜0.05);实时定量PCR和免疫组织化学检测结果表明胆固醇代谢相关基因SREBP2、LDLr和SCAP的mRNA和蛋白质表达水平显著增加. 结论炎症可以通过干扰SREBP-2导致低密度脂蛋白胆固醇摄取异常,造成肝脏脂质沉积增多和损害.     

Effect of apolipoprotein E polymorphism on bile lipid composition and the formation of cholesterol gallstone

OBJECTIVE: It remains a matter of controversy whether possession of the apolipoprotein E4 (apoE4) allele is a genetic risk factor for the formation of cholesterol gallstones. The aim of the present study was to test this hypothesis by investigating the effect of apoE4 on bile lipid composition in normal subjects and in patients with cholesterol gallstones and to evaluate the distributions of apoE alleles in these two groups. METHODS: The study population consisted of 79 patients who underwent open or laparoscopic cholecystectomy for symptomatic cholesterol gallstone disease. The control group (n = 53) included 11 patients with benign gallbladder polyps and 42 normal subjects acting as donors in living donor liver transplantation. The apoE genotypes were assessed by dot blot hybridization with digoxigenin-labeled probes. Bile lipid composition was determined by enzymatic assays and high performance liquid chromatography. RESULTS: Bile lipid composition and cholesterol saturation index (CSI) were similar in the control subjects harboring the apoE4 allele and those without apoE4 (mean CSI, 85.9% and 72.2%, respectively, p = 0.69). Likewise, in the cholesterol gallstone patients, bile lipid composition and CSI were similar in the patients with and without apoE4 allele (mean CSI, 134.9% vs 152.2%, p = 0.6). Furthermore, the prevalence of the apoE4 allele was similar in the patients with cholesterol gallstones and in the control group (8.5% vs 7.6%, p = 0.46, OR = 0.88; 95% CI = 0.64-1.22). CONCLUSIONS: The apoE4 allele is not a contributory factor to cholesterol gallstone formation, at least in the Japanese population.