两株乳杆菌体内外降胆固醇的筛选及相关机制的研究
|
摘要
目的
从正常人肠道粪便中分离的潜在目的菌中筛选出有降胆固醇能力的菌株,并进行鉴定。
方法
通过改良的胆固醇MRS培养基作为筛选模型进行目的菌的筛选,并对降胆固醇能力较好的菌株进行初步鉴定。
结果
经过初筛和复筛,筛选出4株降胆固醇能力在30%以上的菌株,降解率分别为M7-544.7%,M2-134.2%,M10-2-8 32.5%,MM1-16为32.4%；将M7-5和M2-1进行鉴定,M7-5为发酵乳酸杆菌,M2-1为植物乳酸杆菌。
结论
菌株M7-5和M2-1在体外有较强的降胆固醇能力,经鉴定分别为发酵乳杆菌及植物乳杆菌,有待于将其应用于动物体内进行进一步研究。
目的
观察2株乳酸杆菌对高脂饮食喂养的SD大鼠胆固醇代谢的影响,评价其对高脂饮食喂养的SD大鼠降胆固醇作用的有效性和安全性,从而为筛选到有利于人体降胆醇的功能菌提供依据。
方法
40只SD大鼠随机分为4组,K组喂养普通饲料,E、F、I组喂养改良高脂饲料,同时以2株乳酸菌干预,E组是M2-1,F组是M7-5。I组不加益生菌,为高脂模型组,6周末处死大鼠,检测大鼠血脂指标,血清总胆叶酸、肝脂质、粪脂质,体重增加量,Lee指数,肝组织病理学检查及血清谷丙转氨酶等指标。
结果
l、高脂模型组血清TC、TG、LDL-C较正常对照组比均升高(P<0.05),差异有显著性,乳酸菌E组和F组比高脂模型组下降,以F组效果最好,差异有显著性。
2、第4周和第6周,高脂模型组血胆汁酸与正常对照组比升高,但无显著性差异,益生菌E组较高脂模型组下隆,差异有统计学意义。
3、粪胆汁酸和胆固醇高脂模型组升高,与正常对照组比,P<0.05,差异有显著性；乳酸菌E组的胆汁酸和F组的胆固醇均升高,分别与高脂模型组及正常对照组比较,P<0.05,差异有显著性。
4、高脂模型组Lee's指数比正常对照组高,P<0.05,差异有显著性；乳酸菌E组和F组均比高脂模型组低,比正常组高,尤其在第6周,F组与高脂模型组比差异有显著性(P<0.05)。
5、高脂模型组及乳酸菌E组和F组,每周体重增加量较正常对照组高,有显著性差异；第6周乳酸菌F组体重增加量下降,比高脂模型组降低,差异有显著性。
6、肝病理检查HE染色高脂模型组肝脂肪变性较明显,与正常对照组比有显著性差异而乳酸菌E组和F组不明显,与正常对照组无差异。
7、高脂模型组血清谷丙转氨酶升高,但分别与其他各组比较无显著性差异。
结论
1、改良高脂饮食配方连续喂养SD大鼠6周,可以成功造出高脂固醇血症模型。
2、对两株乳杆菌M7-5和M2-1对SD大鼠高脂血症模型有降胆固醇作用,以M7-5效果更好。
3两株乳酸菌可能的降脂机制是减少了肝脂质沉积和增加了粪脂的排泄,它们的机制可能不完全相同,前者以增加粪胆固醇的排泄为主,而后者则以增加粪胆汁酸的排出为主。
目的
探讨两株乳酸菌影响SD大鼠饮食性高脂血症脂质代谢的可能机制
方法
实验动物、分组、建模和干预方法同第2章,第6周末处死大鼠,留取各组肝脏及回肠粘膜上皮标本,用实时荧光定量PCR技术检测肝脏孤核受体FXR及细胞表面受体ABCA1和ABCG5基因mRNA的表达,检测回肠粘膜上皮组织LXRa、ABCA1和ABCG5基因mRNA的表达。
结果
1、高脂模型组,肝组织FXR受体及LXRα受体,回肠粘膜上皮组织LXRα、ABCA1及ABCG5受体与正常对照组比较差异有统计学意义(P<0.05),而肝组织ABCG5表达无明显上调。
2、乳酸菌E组(植物乳肝菌M2-1)肝组织FXR表达与高脂模型组相比显著下调,LXRα则显著上调,回肠粘肠上皮组织细胞表面受体ABCG5上调(P<0.05)。
3、乳酸菌F组(发酵乳杆菌M7-5)肝组织孤核受体FXR与高脂模型组比表达下调,肝组织LXRα、ABCG5,回肠粘膜上皮组织LXRα、ABCA1、ABCG5与高脂膜型组相比均上调,有统计学意义(P<0.05)。
结论
1、发酵乳杆菌M7-5和植物乳杆菌M2-1可降低高脂饮食喂养的SD大鼠血清胆固醇。
2、发酵乳杆菌M7-5和植物乳杆菌M2-1作用靶点可能涉及了肝组织和回肠粘膜的某些受体。前者抑制肝脏FXR的表达,可能上调肝、肠粘膜组织LXR2、ABCA1、ABCG5的表达,降胆固醇作用主要以增加体内胆固醇的排泄为主。后者则显著抑制肝组织FXR的表达,上调肝组织LXRa回肠粘膜上皮组织ABCG5的表达,其降胆固醇作用主要在于增加体内胆汁酸的合成,加速胆汁酸的排泄为主。
Objective
To screen the strains with the capability to reduce cholesterol from the potential target bacteria isolated by stool samples of healthy adults and identify them.
Methods
We screen the potential target bacteria through modified cholesterol MRS medium as the screening model, and preliminary identify the strains with relative strong capability to cholesterol-reducing
Results
Screened out four strains with the 30% or more capability to cholesterol-reducing, with degradation rates M7-5 44.7%, M2-1 34.2%, M10-2-8 32.5%, and MM1-16 32.4% respectively. Identify M7-5 and M2-1 and M7-5 is Lactobacillus fermentum, M2-1 is Lactobacillus plantarum.
Conclusion
M7-5 and M2-1 had strong capability to cholesterol-reducing in vitro, The result of identification shows that M7-5 and M2-1 were Lactobacillus fermentum, and Lactobacillus plantarum., respectively and
we need Further Study of them to apply them to the animals in vivo.
Objective
To observe the effect of two strains of lactobacilli on the Cholesterol metabolism of the male Sprague-Dawley rats fed with high-fat diet and to evaluate their efficacy and safety on lowing cholesterol levels, so as to provide support for screening bacteria that could reduce cholesterol.
Method
40 SD rats were randomly divided into 4 groups, K, E, F and I group. K group was normal group fed with the normal diet, E group was interfered with high fat diet and lactobacillus M2-1, F group was interfered with high fat diet and lactobacillus M7-5.Ⅰgroup was model group, interfered with high fat diet only. All rats were sacrificed in the 6th week, then the levels of serum lipids, serum total bile acids, total cholesterol, liver lipids, fecal lipids, weight gain, Lee's index, liver histopathology, serum glutamic-pyruvic transaminase and other index were detected.
Results
1. Interfered with lactobacilli, levels of serum TC, TG and LDL-C in the E and F group were lower compared with the model group, and higher compared with the normal group. The difference was significant. Effect of the M7-5 was the best, the difference was significant.
2. In the 4th and 6th week, levels of serum bile acid in the E group was higher compared with the normal group (P>0.05), and was lower compared with the model group(P<0.05).
3. Levels of fecal bile acids and cholesterol in the model group were higher compared with the normal group(P<0.05), the difference was significant. Bile acid Level in the E group was higher compared with the model group. Cholesterol Level was lower compared with the normal group. The difference was significant.
4. Lee's index of model group was higher compared with the normal group (P<0.05). It was lower in the model group and higher in the normal group compared with Lactobacillus E and F group. Especially in the 6th week, difference was significant between the F and I group (P <0.05).
5. weight gain daily in the model and Lactobacillus groups was higher compared with the normal group, difference was significant; From the 6th week, weight gain in the F group decreased. It was lower compared with the model group (P<0.05). Difference was significant.
6. Adipose degeneration was very obvious in the model group and very slight in the Lactobacillus E and F groups with the method of HE staining of fatty liver
7. Serum bile acid in the model group were increased, but there was no difference between the model and other groups.
Conclusion
1. Feeding the SD rats continuously with modified improvement compounding of high-fat diet for 6 weeks could successfully induce model of hyperlipoidemia, especially hypercholesterolemia.
2. Two strains of Lactobacillus M7-5 and M2-1 could low the level of hyperlipemia in the SD model.M7-5 had a better effect.
3. The possible mechanism of the two strains of Lactobacillus lowerng the hyperlipoidemia might be decreasing the deposition of liver lipid and increasing the excretion of fecal fat. Their mechanism might not be exactly the same. The former might be mostly increasing the excretion of the fecal cholesterol and the latter increasing the excretion of the fecal bile acid.
Objective
Investigate possible affection mechanism of SD rats alimentary hyperlipoidemia by two lactobacillus
Methods
Test animals、group、group and intervention are same as the 2nd chapter, rats were executed after the 6th week, specimen of liver and ileal mucous membrane mucosae were kept to test expression of liver nuclear receptor FXR and cell surface receptor ABCA1 and ABCG5 mRNA, and expression of ileal mucous membrane mucosae LXRa,ABCA1 and ABCG5.
Results
1. Liver receptor FXR and LXRa, ileal mucous membrane mucosae LXRa, ABCA1 and ABCG5 in hyperlipoidemia group were obvious different with normal group (P<0.05), but liver ABCG5 were not obviously up-regulated.
2. In E group of lactobacillus, liver receptor FXR were obviously down-regulated and LXRa were obviously up-regulated, ileal mucous membrane mucosae surface receptor ABCG5 were up-regulated in liver tissue.
3.In F group of lactobacillus, liver nuclear receptor FXR were obviously down-regulated and LXRα、ABCG5、ileal mucous membrane mucosae surface receptor LXRα、ABCA1 and ABCG5 were obviously up-regulated with statistics significance compared to hyperlipoidemia group (P<0.05)
Conclusion
1. Lactobacillus fermentum M7-5 and Lactobacillus plantarum M2-1 can degrade serum cholesterol in high fat diet SD rats.
2.Affection target of Lactobacillus fermenti M7-5 and Lactobacillus fermenti M2-1 possible related with hepatic tissue and receptors in ileal mucous. the fronter depressed FXR expression of liver and up-regulated expression of LXRα、ABCA1 and ABCG5 in mucous tissue in liver and ileal which leads to the enhancing of cholesterol excretion. the later obviously depressed FXR expression of liver and up-regulated expression of LXRa in liver and ABCG5 in ileal mucous membrane which enhance the synthesis of bile acid and cholesterol excretion to down-regulate cholesterol
从正常人肠道粪便中分离的潜在目的菌中筛选出有降胆固醇能力的菌株,并进行鉴定。
方法
通过改良的胆固醇MRS培养基作为筛选模型进行目的菌的筛选,并对降胆固醇能力较好的菌株进行初步鉴定。
结果
经过初筛和复筛,筛选出4株降胆固醇能力在30%以上的菌株,降解率分别为M7-544.7%,M2-134.2%,M10-2-8 32.5%,MM1-16为32.4%；将M7-5和M2-1进行鉴定,M7-5为发酵乳酸杆菌,M2-1为植物乳酸杆菌。
结论
菌株M7-5和M2-1在体外有较强的降胆固醇能力,经鉴定分别为发酵乳杆菌及植物乳杆菌,有待于将其应用于动物体内进行进一步研究。
目的
观察2株乳酸杆菌对高脂饮食喂养的SD大鼠胆固醇代谢的影响,评价其对高脂饮食喂养的SD大鼠降胆固醇作用的有效性和安全性,从而为筛选到有利于人体降胆醇的功能菌提供依据。
方法
40只SD大鼠随机分为4组,K组喂养普通饲料,E、F、I组喂养改良高脂饲料,同时以2株乳酸菌干预,E组是M2-1,F组是M7-5。I组不加益生菌,为高脂模型组,6周末处死大鼠,检测大鼠血脂指标,血清总胆叶酸、肝脂质、粪脂质,体重增加量,Lee指数,肝组织病理学检查及血清谷丙转氨酶等指标。
结果
l、高脂模型组血清TC、TG、LDL-C较正常对照组比均升高(P<0.05),差异有显著性,乳酸菌E组和F组比高脂模型组下降,以F组效果最好,差异有显著性。
2、第4周和第6周,高脂模型组血胆汁酸与正常对照组比升高,但无显著性差异,益生菌E组较高脂模型组下隆,差异有统计学意义。
3、粪胆汁酸和胆固醇高脂模型组升高,与正常对照组比,P<0.05,差异有显著性；乳酸菌E组的胆汁酸和F组的胆固醇均升高,分别与高脂模型组及正常对照组比较,P<0.05,差异有显著性。
4、高脂模型组Lee's指数比正常对照组高,P<0.05,差异有显著性；乳酸菌E组和F组均比高脂模型组低,比正常组高,尤其在第6周,F组与高脂模型组比差异有显著性(P<0.05)。
5、高脂模型组及乳酸菌E组和F组,每周体重增加量较正常对照组高,有显著性差异；第6周乳酸菌F组体重增加量下降,比高脂模型组降低,差异有显著性。
6、肝病理检查HE染色高脂模型组肝脂肪变性较明显,与正常对照组比有显著性差异而乳酸菌E组和F组不明显,与正常对照组无差异。
7、高脂模型组血清谷丙转氨酶升高,但分别与其他各组比较无显著性差异。
结论
1、改良高脂饮食配方连续喂养SD大鼠6周,可以成功造出高脂固醇血症模型。
2、对两株乳杆菌M7-5和M2-1对SD大鼠高脂血症模型有降胆固醇作用,以M7-5效果更好。
3两株乳酸菌可能的降脂机制是减少了肝脂质沉积和增加了粪脂的排泄,它们的机制可能不完全相同,前者以增加粪胆固醇的排泄为主,而后者则以增加粪胆汁酸的排出为主。
目的
探讨两株乳酸菌影响SD大鼠饮食性高脂血症脂质代谢的可能机制
方法
实验动物、分组、建模和干预方法同第2章,第6周末处死大鼠,留取各组肝脏及回肠粘膜上皮标本,用实时荧光定量PCR技术检测肝脏孤核受体FXR及细胞表面受体ABCA1和ABCG5基因mRNA的表达,检测回肠粘膜上皮组织LXRa、ABCA1和ABCG5基因mRNA的表达。
结果
1、高脂模型组,肝组织FXR受体及LXRα受体,回肠粘膜上皮组织LXRα、ABCA1及ABCG5受体与正常对照组比较差异有统计学意义(P<0.05),而肝组织ABCG5表达无明显上调。
2、乳酸菌E组(植物乳肝菌M2-1)肝组织FXR表达与高脂模型组相比显著下调,LXRα则显著上调,回肠粘肠上皮组织细胞表面受体ABCG5上调(P<0.05)。
3、乳酸菌F组(发酵乳杆菌M7-5)肝组织孤核受体FXR与高脂模型组比表达下调,肝组织LXRα、ABCG5,回肠粘膜上皮组织LXRα、ABCA1、ABCG5与高脂膜型组相比均上调,有统计学意义(P<0.05)。
结论
1、发酵乳杆菌M7-5和植物乳杆菌M2-1可降低高脂饮食喂养的SD大鼠血清胆固醇。
2、发酵乳杆菌M7-5和植物乳杆菌M2-1作用靶点可能涉及了肝组织和回肠粘膜的某些受体。前者抑制肝脏FXR的表达,可能上调肝、肠粘膜组织LXR2、ABCA1、ABCG5的表达,降胆固醇作用主要以增加体内胆固醇的排泄为主。后者则显著抑制肝组织FXR的表达,上调肝组织LXRa回肠粘膜上皮组织ABCG5的表达,其降胆固醇作用主要在于增加体内胆汁酸的合成,加速胆汁酸的排泄为主。
Objective
To screen the strains with the capability to reduce cholesterol from the potential target bacteria isolated by stool samples of healthy adults and identify them.
Methods
We screen the potential target bacteria through modified cholesterol MRS medium as the screening model, and preliminary identify the strains with relative strong capability to cholesterol-reducing
Results
Screened out four strains with the 30% or more capability to cholesterol-reducing, with degradation rates M7-5 44.7%, M2-1 34.2%, M10-2-8 32.5%, and MM1-16 32.4% respectively. Identify M7-5 and M2-1 and M7-5 is Lactobacillus fermentum, M2-1 is Lactobacillus plantarum.
Conclusion
M7-5 and M2-1 had strong capability to cholesterol-reducing in vitro, The result of identification shows that M7-5 and M2-1 were Lactobacillus fermentum, and Lactobacillus plantarum., respectively and
we need Further Study of them to apply them to the animals in vivo.
Objective
To observe the effect of two strains of lactobacilli on the Cholesterol metabolism of the male Sprague-Dawley rats fed with high-fat diet and to evaluate their efficacy and safety on lowing cholesterol levels, so as to provide support for screening bacteria that could reduce cholesterol.
Method
40 SD rats were randomly divided into 4 groups, K, E, F and I group. K group was normal group fed with the normal diet, E group was interfered with high fat diet and lactobacillus M2-1, F group was interfered with high fat diet and lactobacillus M7-5.Ⅰgroup was model group, interfered with high fat diet only. All rats were sacrificed in the 6th week, then the levels of serum lipids, serum total bile acids, total cholesterol, liver lipids, fecal lipids, weight gain, Lee's index, liver histopathology, serum glutamic-pyruvic transaminase and other index were detected.
Results
1. Interfered with lactobacilli, levels of serum TC, TG and LDL-C in the E and F group were lower compared with the model group, and higher compared with the normal group. The difference was significant. Effect of the M7-5 was the best, the difference was significant.
2. In the 4th and 6th week, levels of serum bile acid in the E group was higher compared with the normal group (P>0.05), and was lower compared with the model group(P<0.05).
3. Levels of fecal bile acids and cholesterol in the model group were higher compared with the normal group(P<0.05), the difference was significant. Bile acid Level in the E group was higher compared with the model group. Cholesterol Level was lower compared with the normal group. The difference was significant.
4. Lee's index of model group was higher compared with the normal group (P<0.05). It was lower in the model group and higher in the normal group compared with Lactobacillus E and F group. Especially in the 6th week, difference was significant between the F and I group (P <0.05).
5. weight gain daily in the model and Lactobacillus groups was higher compared with the normal group, difference was significant; From the 6th week, weight gain in the F group decreased. It was lower compared with the model group (P<0.05). Difference was significant.
6. Adipose degeneration was very obvious in the model group and very slight in the Lactobacillus E and F groups with the method of HE staining of fatty liver
7. Serum bile acid in the model group were increased, but there was no difference between the model and other groups.
Conclusion
1. Feeding the SD rats continuously with modified improvement compounding of high-fat diet for 6 weeks could successfully induce model of hyperlipoidemia, especially hypercholesterolemia.
2. Two strains of Lactobacillus M7-5 and M2-1 could low the level of hyperlipemia in the SD model.M7-5 had a better effect.
3. The possible mechanism of the two strains of Lactobacillus lowerng the hyperlipoidemia might be decreasing the deposition of liver lipid and increasing the excretion of fecal fat. Their mechanism might not be exactly the same. The former might be mostly increasing the excretion of the fecal cholesterol and the latter increasing the excretion of the fecal bile acid.
Objective
Investigate possible affection mechanism of SD rats alimentary hyperlipoidemia by two lactobacillus
Methods
Test animals、group、group and intervention are same as the 2nd chapter, rats were executed after the 6th week, specimen of liver and ileal mucous membrane mucosae were kept to test expression of liver nuclear receptor FXR and cell surface receptor ABCA1 and ABCG5 mRNA, and expression of ileal mucous membrane mucosae LXRa,ABCA1 and ABCG5.
Results
1. Liver receptor FXR and LXRa, ileal mucous membrane mucosae LXRa, ABCA1 and ABCG5 in hyperlipoidemia group were obvious different with normal group (P<0.05), but liver ABCG5 were not obviously up-regulated.
2. In E group of lactobacillus, liver receptor FXR were obviously down-regulated and LXRa were obviously up-regulated, ileal mucous membrane mucosae surface receptor ABCG5 were up-regulated in liver tissue.
3.In F group of lactobacillus, liver nuclear receptor FXR were obviously down-regulated and LXRα、ABCG5、ileal mucous membrane mucosae surface receptor LXRα、ABCA1 and ABCG5 were obviously up-regulated with statistics significance compared to hyperlipoidemia group (P<0.05)
Conclusion
1. Lactobacillus fermentum M7-5 and Lactobacillus plantarum M2-1 can degrade serum cholesterol in high fat diet SD rats.
2.Affection target of Lactobacillus fermenti M7-5 and Lactobacillus fermenti M2-1 possible related with hepatic tissue and receptors in ileal mucous. the fronter depressed FXR expression of liver and up-regulated expression of LXRα、ABCA1 and ABCG5 in mucous tissue in liver and ileal which leads to the enhancing of cholesterol excretion. the later obviously depressed FXR expression of liver and up-regulated expression of LXRa in liver and ABCG5 in ileal mucous membrane which enhance the synthesis of bile acid and cholesterol excretion to down-regulate cholesterol
引文
[1]Hjermann, I. Intervention of smoking and eating habits in healthy men carrying high risk for coronary heart disease.The Oslo Study. Acta Med Scand Suppl 1981, 651:281-284.
[2]杨诗杰,苏汝好,项岚等,降血脂药的应用现状及研究进展,医药论坛杂志,2006,27(1)：90-92
[3]Kajinami K, Takekoshi N. Cholesterol absorption inhibitors in development as potential therapeutics. Expert Opin Investig Drugs,2002,21 (3):831-835.
[4]Mann, G. V., Spoerry, A., Gray, M.& Jarashow, D. Atherosclerosis in the Masai. Am J Epidemiol,1972,95:26-37.
[5]Lin DC.Probiotics as functional foods.Nutr Clin Pract.2003,8(6):497-506.
[6]Larkin TA, Astheimer LB, Price WE.Dietary combination of soy with a probiotic or prebiotic food significantly reduces total and LDL cholesterol in mildly hypercholesterolaemic subjects.Eur J Clin Nutr.2007 Oct 17:236-239
[7].韩俊华,盛晓甘.乳酸菌降胆固醇作用的现状,中国乳品工业,2002,30(3)：16-20。
[8]Jaspers.D.A.Linda K.M, Lloyd.D.L.Effect of consuming yogurts prepared with three culture strains on human serum lipoproteins.Journal Food Science,1984,49:1178-1181.
[9]郑坚.乳酸菌对血脂的影响.黄冈师范学院学报,2002,22(3)：37-53
[10]Pereira.D.I. Gibson.GR. Effects of consumption of probiotics and prebiotics on serum lipid level in humans. Crit Rev Biochem Mol Biol,2002,37 (4):259-281.
[11]Gilliland.S.E, Nelson.C.R and Maxwel L C. Assilation of cholesterol by Lactobacillus acidophilus. Appl. Envi Micr,1985,49:377-381
[12]Buck.L.M, Gilliland.S.E. Comparisons of freshly isolated strains of Lactobacillus acidophilus of human intestinal origin for ability to assimilate cholesterol during growth.J Dairy Sci,1994,77:2925-2933.
[13]Dambekodi P.C. Gilliland S.E. Incorporation of cholesterol into the cellula membrane of bifidobacterium longurn. J dairy Sci.1998,81:1818-1824
[14]Don.D.O, Kim S.H, Gilliland S.E. Incorporation of cholesterol into the cell membrane of Lactobacillus acidophilus ATCC 43121.J Dairy Sci,1997,80: 3107-3113.
[15]Thome K.D. Barker.D.C.The occurrence of bactoprenol in the mesosome and plasma membranes of Lactobacillus casei and Lactobacillus plantarum.J Gen Microbiol,1972,70:87
[16]Zhao JR, Yang H.Progress in the effect of probiotics on cholesterol and its mechanism.Wei Sheng Wu Xue Bao.2005,45(2):315-319.
[17]Pereira DI, McCartney AL, Gibson GR.An in vitro study of the probiotic potential of a bile-salt-hydrolyzing Lactobacillus fermentum strain, and determination of its cholesterol-lowering properties. Appl Environ Microbiol.2003,69(8):4743-52.
[18]Buck L M, Gilliland S E. Comparisons of freshly isolated strans of lactobacillus Acidophilus of human in testinal origin for ability to assimilate cholesterol during growth..J Dairy Sei,1994,77:2925-2933
[19]Mott G E. Lowering of serum cholesterol by intestinal bacteria in cholesterol-fed piglets. Lipids,1993(8):428
[20]Tarant M P, Seama F. Bile salt hydrolase plays a key role on cholesterol removal by Lactobacillus reuteri. Biotechnol Lett,1997,19:845-47
[21]Dilmi-Bouras A.Assimilation (in vitro) of cholesterol by yogurt bacteria. Ann Agric Environ Med.2006,13(1):49-53.
[22]Grill JP, Cayuela C, Antoine JM, et al.Effects of Lactobacillus amylovorus and Bifidobacteria breve on cholesterol. Lett Appl Microbiol.,2000, Aug:31(2):154-156.
[23]Park YH, Kim JG, Shin YW,et al. Effect of dietary inclusion of Lactobacillus acidophilus ATCC 43121 on cholesterol metabolism in rats.J Microbiol Biotechnol. 2007,17(4):655-662.
[24]Han KH, Iijuka M, Shimada K, et al. Adzuki resistant starch lowered serum cholesterol and hepatic 3-hydroxy-3-methylglutaryl-CoA mRNA levels and increased hepatic LDL-receptor and cholesterol 7alpha-hydroxylase mRNA levels in rats fed a cholesterol diet.Br J Nutr,2005,94(6):902-908.
[25]Shima T, Fukushima K, Setoyama H,et al. Differential effects of two probiotic strains with different bacteriological properties on intestinal gene expression, with special reference to indigenous bacteria.FEMS Immunol Med Microbiol, 2008,52(1):69-77.
[26]Clee SM, Zwinderman AH, Engert JC, et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease[J]. Circulation,2001,103 (1):198-205
[27]Tang CK, Yi GH, Yang JH, et al. Oxidized LDL upregulated ATP binding cassette transporter-1 in T'HP-1 macrophages[J]. Acta Pharmaeol Sin,2004; 25(5): 581-586.
[28]Feng B. Tabas I. ABCA 1-mediated cholesterol efflux is defectivein free cholesterol-loaded maerophages. Mechanism involves enhanced ABCA 1 degradation in a process requiring full NPC1 activity. J Biol Chem,2002,277 (45):43271-43280
[29]de Vogel-van den Bosch, H. M. et al. A cholesterol-free, high-fat diet suppresses gene expression of cholesterol transporters in murine small intestine. Am J Physiol Gastrointest Liver Physiol 2008,294,G1171-1180
[30]Schwart K, Lawn RM, Wade DP. ABC 1 gene expression and Apo-A1 mediated cholesterol sterol efflux are regulated by LXR. Biochem Biophys Res Commun, 2000.274(3):794-802
[31]Wade DP, Owen JS. Regulation of the cholesterol efflux geneABCA1. Lancet, 2001,357(9251):161-163
[32]Huuskonen J, Vishnu M, Pullinger CR, et al. Regulation of ATP-binding cassette transporter Al transcription by thyroidhormone receptor. Biochemistry,2004,43 (6): 1626-1632
[33]Luo Y, Tall AR. Sterol upregulation of human CETP expressionin vitro and in transgenic mice by an LXR element. J Clin Invest,2000,105(4):513-520
[34]Francis G.A, Knopp R.H. Oram J.F. Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease.J.Clin.Invest.1995,96:78-87
[35]Lee MH, Lu K, Hazard S, et al.Identification of a gene, ABCG5, important in the regulation of dietary cholesterol absorption. Nat Genet,2001,27 (1):79-83.
[36]Lu k, Lee MH, Hazard S, et al. Two genes that map to the STSL locus cause sitosterolemia:genomic structure and spectrum of mutations involving sterolin-1 and sterolin-2, encoded by ABCG5 and ABCG8, respectively. Am J Hum Genet,2001,69 (2):278-290
[37]Berge KE, Tian H, Graf GA, et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters. Science,2000,290 (5497):1771-1775.
[38]Yu L, Li-Hawkins J, Hammer RE, et al. Overexpression of ABCG5 and ABCG8 promotes biliary cholesterol secretion and reduces fractional absorption of dietary cholesterol. J Clin Invest,2002,110 (5):671-680.
[39]Yu L, Hammer RE, Li-Hawkins J, et al. Disruption of Abcg5 and Abcg8 in mice reveals their crucial role in biliary cholesterol secretion. Proc Natl Acad Sci USA, 2002,99(25):16237-16242.
[40]Yu L, Gupta S, Xu F, et al. Expression of ABCG5 and ABCG8 is required for regulation of biliary cholesterol secretion. J Biol Chem,2005,280 (10):8742-8747.
[41]Duan LP, Wang HH, Wang DQ. Cholesterol absorption is mainlyregulated by the jejunal and ileal ATP-binding cassette sterol efflux transporters Abcg5 and Abcg8 in mice. J Lipid Res,2004,45 (7):1312-1323.
[42]Yu L, York J, von Bergmann K, et al. Stimulation of cholesterol excretion by the liver X receptor agonist requires ATP-binding cassette transporters G5 and G8. J Biol Chem,2003,278 (18):15565-15570.
[43]Repa JJ, Berge KE, Pomajzl C, et al. Regulation of ATP-bindingcassette sterol transporters ABCG5 and ABCG8 by the liver X receptors αand β. J Biol Chem,2002, 277(21):18793-18800.
[44]Shulman AI, Mangelsdorf DJ. Retinoid X receptor heterodimers in the metabolic syndrome. N Engl J Med,2005,353:604-615.
[44.1]赵瑞香,孙俊良,李明静,等.嗜酸乳杆菌同化MRS培养金中胆固醇能力的研究.中国微生态杂志,2005,17(4)：254-255
[45]刘丽莉,董铁有,杨协力.6种乳酸菌降胆固醇的体外实验.河南科技大学学报(自然科学版),2005,26(6)：85-88
[46]Reddy, K. B., Raghavendra, P., Kumar, B. G., et al. Screening of probiotic properties of lactic acid bacteria isolated from Kanjika, an ayruvedic lactic acid fermented product:an in-vitro evaluation. J Gen Appl Microbiol,2007,53,207-213
[47]香卫钦,于舒宁,张耀林,等.一株能降解胆固醇的乳酸菌的选育.生物技术,2001,11(05)：9-10
[48]肖琳琳,董明盛.西藏干酪乳酸菌降胆固醇特性研究.食品科学,2003,24(10)：142-145
[49]Gerard, P. Lepercq, P. Leclerc M, et al. Bacteroides sp. strain D8, the first cholesterol-reducing bacterium isolated from human feces. Appl Environ Microbiol 2007,73:5742-5749
[50]Mariat, D. The Firmicutes/Bacteroidetes ratio of the human microbiota changes with age. BMC Microbiol 2009,9:123,1471-2180
[51]Pfeiler EA, Klaenhammer TR.The genomics of lactic acid bacteria.Trends Microbiol,2007,15(12):546-553.
[52]Ljungh A, Wadstrom T.Lactic acid bacteria as probiotics. Curr Issues Intest Microbiol,2006,7(2):73-89.
[53]Ganzle MG, Vermeulen N, Vogel RF.Carbohydrate, peptide and lipid metabolism of lactic acid bacteria in sourdough. Food Microbiol,2007,24(2):128-138.
[54]Furzikova, T. M., Sorokulova, I. B., Serhiichuk, M. H., et al.The effect of antibiotic preparations and their combinations with probiotics on the intestinal microflora of mice. Mikrobiol Z,2000,62:26-35.
[55]Tannock, G. W., Tangerman, A., Van Schaik, A.et al. Deconjugation of bile acids by lactobacilli in the mouse small bowel. Appl Environ Microbiol,1994,60, 3419-3420.
[56]Pereira, D. I. Gibson, G. R. Cholesterol assimilation by lactic acid bacteria and bifidobacteria isolated from the human gut. Appl Environ Microbiol,2002,68, 4689-4693
[57]Klaver, F. A.& van der Meer, R. The assumed assimilation of cholesterol by Lactobacilli and Bifidobacterium bifidum is due to their bile salt-deconjugating activity. Appl Environ Microbiol,1993,59,1120-1124.
[58]Brashears MM, Gilliland SE, Buck LM.Bile salt deconjugation and cholesterol removal from media by Lactobacillus casei. J Dairy Sci.1998,81(8):2103-2110.
[59]郑建仙.功能性食品.第三卷.北京,中国轻工业出版社,2001：275-289
[60]徐叔云,卞如濂,陈修.药理实验方法学[M].第3版.北京：人民卫生出版社,2003,189-190
[61]Lin, C. Y., Tsai, C. Y. Lin, S. H. Effects of soy components on blood and liver lipids in rats fed high-cholesterol diets. World J Gastroenterol,2005,11:5549-5552
[62]Lepercq P, Relano P, Cayuela C, et al. Bifidobacteria animalis strain DN-173 010 hydrolyses bile salts in the gastrointestinal tract of pigs. Scand J Gastroenterol.2004, 39(12):1266-1271.
[63]石如玲,赵朝贤,朱海暴,等。大鼠胆汁酸合成加强时肝脏双功能蛋白mRNA表达及活性升高.基础医学与临床,2006,26(7)：720-723
[64]Kajiura K, Ohkusa T, Okayasu I. Relationship between fecal bile acids and the occurrence of colorectal neoplasia in experimental murine ulcerative colitis.Digestion. 1998; 59 (1):69-72.
[65]申瑞玲,董吉林,李文全.燕麦p-葡聚糖对高脂血症大鼠胆固醇代谢的影响.中国食品学报,2009,9(3)：14-19
[66]Fukada Y, Kimura K,Ayaki Y.Effect of chitosan feeding on intestinal bile acid metabolism in rats[J].Lipids,1991:395-399
[67]薛琨,郭红卫,陈凤麟,中链脂肪酸对营养性肥胖大鼠体重及脂质代谢的作用,卫生研究,2006,35(2)：187-190
[68]Moghadasian, M. H., Frohlich, J. J. McManus, B. M. Advances in experimental dyslipidemia and atherosclerosis. Lab Invest,2001,81:1173-1183
[69]陈凯,张雁芳,王倩,等.高胆固醇饲养兔鹤鹑和大鼠诱发高血脂和动脉粥样硬化的特征.解放军药学学报,2001,117-124.
[70]Boehler, N. et al. Antilithiasic effect of beta-cyclodextrin in LPN hamster: comparison with cholestyramine. J Lipid Res,1999,40:726-734
[71]Osono, Y., Woollett, L. A., Herz, J.& Dietschy, J. M. Role of the low density lipoprotein receptor in the flux of cholesterol through the plasma and across the tissues of the mouse. J Clin Invest,1995,95:1124-1132
[72]Spady, D. K.& Cuthbert, J. A. Regulation of hepatic sterol metabolism in the rat. Parallel regulation of activity and mRNA for 7 alpha-hydroxylase but not 3-hydroxy-3-methylglutaryl-coenzyme A reductase or low density lipoprotein receptor. J Biol Chem,1992,267:5584-5591
[73]Bhathena, J., Martoni C., Kulamarva, A., et al. Orally delivered microencapsulated live probiotic formulation lowers serum lipids in hypercholesterolemic hamsters. J Med Food,2009,12(2):310-319.
[74]Kim, N. H., Moon. P. D., Kim, S. J, et al. Lipid profile lowering effect of Soypro fermented with lactic acid bacteria isolated from Kimchi in high-fat diet-induced obese rats. Biofactors,2008,33(1):49-60.
[75]Fukushima, M.& Nakano, M. Effects of a mixture of organisms, Lactobacillus acidophilus or Streptococcus faecalis on cholesterol metabolism in rats fed on a fat-and cholesterol-enriched diet. Br J Nutr,1996,76:857-867
[76]Keim N L, Marlett J A, Amundsopn C H. The cholesterolemic effect of skim milk in young men consuming controlled diets[J].Nutrition research,1981, 1:422-429.
[77]Rossouw, J. E., Burger, E. M., Van der Vyver, P. et al.The effect of skim milk, yoghurt, and full cream milk on human serum lipids. Am J Clin Nutr,1981,34: 351-356.
[78]Hashimoto H, Yamazaid K, He F, et al. Hypocholesterolemic effects of Lactobacillus casei subsp. casei TMC 0409 strain observed in rats fed cholesterol contained diets[J].Animal Science Journal,1999,72:90-97.
[79]任邦哲等.生物化学与临床医学.长沙,湖南科学技术出版社,1992：202-206
[80]Nomiyama T.Bruemmer D. Liver X receptors as therapeutic targets in metabolism and atherosclerosis. Curr Atheroscler Rep,2008,10:88-95.
[81]Clee SM, Zwinderman AH, Engert JC, et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease[J]. Circulation,2001,103(1):198-205.
[82]Tang CK, Yi GH, Yang JH, et al. Oxidized LDL upregulated ATP binding cassette transporter-1 in T'HP-1 macrophages[J]. Acta Pharmaeol Sin,2004; 25(5): 581-6.
[83]Francis,GA.,Knopp,R.H. Oram,J.F. Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease.J.Clin.Invest.1995,96:78-87
[84]Repa, J. J., Turley, S. D., Laboccaro, J.-M.A., et al. Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers. Science (Washington, DC) 2000,289:1524-1529.
[85]Berge, K. E., Tian, H., Graf, G. A., et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters.Science (Washington, DC),2000,290:1771-1775.
[86]Osono, Y., Woollett, L. A., Herz, J.& Dietschy, J. M. Role of the low density lipoprotein receptor in the flux of cholesterol through the plasma and across the tissues of the mouse. J Clin Invest,1995,95:1124-1132
[87]Spady, D. K.& Cuthbert, J. A. Regulation of hepatic sterol metabolism in the rat. Parallel regulation of activity and mRNA for 7 alpha-hydroxylase but not 3-hydroxy-3-methylglutaryl-coenzyme A reductase or low density lipoprotein receptor. J Biol Chem,1992,267:5584-5591.
[88]Costet, P., Luo, Y., Wang, N. et al. Sterol-dependent transactivation of the ABC1 promoter by the liver X receptor/retinoid X receptor.J. Biol Chem,2000,275: 28240-28245.
[89]Edwards PA. Kast HR, Anisfeld AM, et al.The adoption of LXR and FXR and their roles in lipid homeostasis J Lipid Res,2002,43(1):2-12.
[90]Repa, J. J., Dietschy, J. M. Turley, S. D.et al. Inhibition of cholesterol absorption by SCH 58053 in the mouse is not mediated via changes in the expression of mRNA for ABCA1, ABCG5, or ABCG8 in the enterocyte. J. Lipid Res.2002,43:1864-1874.
[91]Repa, J.J, Liang G, Ou J, et al. Regulation of mouse sterol regulatory element-binding protein-lc gene (SREBP-1c) by oxysterol receptors, LXRa and LXRp. Genes Dev,2000,14:2819-2830.
[1]任邦哲等.生物化学与临床医学.长沙,湖南科学技术出版社,1992：202-206
[2]Peet DJ, lanowski BA, Mangelsdorf DI.111e LXRs:a new class of oxysterol receptors. Curr Opin Genet Dev 1998; 8:571-575
[3]Willy, P. J. et al. LXR, a nuclear receptor that defines a distinct retinoid response pathway. Genes Dev 9,1033-1045 (1995).
[4]Bjorkhem I, Diczfalusy U.24(S),25-Epoxycholesterol-A Potential Friend.[J].Arteriosclerosis,Thrombosis&Vascular Biology.2004,24(12):2209-2210.
[5]Rowe AH, Argmann CA, Edwards JY,et al. Enhanced synthesis of the oxysterol 24(S),25-epoxycholesterol on macrophages by inhibitors of 2, 3-oxidosqualene:lanosterol cyclase.[J].Circulation Research.2003,93:717-725.
[6]Fu X, Menke JG, Chen Y, et al.27-hydroxycholesterol is an endogenous ligand for liver X receptor in cholesterol-loaded cells.[J].Biol.Chem.2001,276:38378-38387.
[7]Colombo J, Kannass KN, Shaddy DJ, et al. Maternal DHA and the development of attention in infancy and toddlerhood. Child Dev,2004,75(4):1254-1267
[8]Song C, Liao S.Cholestenoic acid is a naturally occurring ligand for liver X receptor alpha.[J].Endocrinology 2000,141:4180-4184.
[9]Sparrow CP,Baffic J,Lam MH,et al.A potent synthetic LXR agonist is more effectivethan cholesterol loading at inducing ABCA1 mRNA and stimulating cholesterol efflux.[J].Biol.Chem.2002,277:10021-10027.
[10]Joseph SB, McKilligin E, Pei L,et al. Synthetic LXR ligand inhibits the development of atherosclerosis in mice.[J].Proc.Natl.Acad.Sci.U.S.A,2002, 99:7604-7609.
[11].Song C,Hiipakka RA,Liao S.Selective activation of liver X receptor alpha by6alpha-hydroxy bile acids and analogs.[J].Steroids.2000,65:423-427.
[12]Janowski BA,Grogan MJ,Jones SA,et al.Structural requirements of ligands for the oxysterol liver X receptors LXRalpha and LXRbeta [J]. Proc.Natl.Acad.Sci.U.S.A.1999,96:266-271.
[13]Zelcer N, Tontonoz P. Liver X receptors as integrators of metabolic and inflammatory signaling. J Clin Invest,2006,116:607-614
[14]Geyeregger R, Zeyda M, Stulnig TM, et al. Liver X receptors in cardiovascular and metabolic disease. Cell Mol Life Sci,2006:63:524-539
[15]Shulman AI, Mangelsdorf DJ.Retinoid X receptor heterodimers in the metabolic syndrome. N Engl J Med,2005,353:604-615.
[16]Laffitte BA, Repa JJ, Joseph SB, et al. LXRs control lipid-inducible expression of apolipo-protein E gene in macrophages and adipose tissue. Proe Natl Acad Sci USA,2001,98:507-512.
[17]Ishimoto K Tachibana K, Sumitomo M, et al. Identification of human low-density lipoprotein receptor as a novel target gene regulated by liver X receptor alpha. FEBS Lett,2006,580:4929-4933
[18]Brown MS, Goldstein JL. The SREBP pathway:regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor [J].Cell,1997, 89:331-340.
[19]Horton JD, Goldstein JL, Brown MS. SREBPs:activators of the complete program of cholesterol and fatty acid synthesis in the liver [J]. Clin Invest.2002, 109:1125-1131.
[20]Peet DJ, Turley SD, Ma W, et al. Cholesterol and bile acid metabolism are impaired in mice lacking the nuclear oxysterol receptor LXR alpha.[J].Cell,1998, 93:693-704.
[21]Alberti S, Schuster GU, Parini P, et al. Hepatic cholesterol metabolism and resistance to dietary cholesterol in LXRbeta-deficient mice.[J].Clin.Invest.2001, 107:565-573.
[22]Schultz JR, Tu H, Luk A, et al. Role of LXRs in control of lipogenesis [J].Genes Dev.2000,14:2831-2838.
[23]Song C, Hiipakka RA, Liao S. Auto-oxidized cholesterol sulfates are antagonistic ligands of liver X receptors:implications for the development and treatment of atherosclerosis.[J].Steroids.2001,66:473-479.
[24]Berge KE, Tian H, Graf GA, et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters. [J]. Science,2000, 90:1771-1775.
[25]Yu L, York J, von Bergmann K, et al. Stimulation of cholesterol excretion by the liver X receptor agonist requires ATP-binding cassette transporters G5 and G8. [J]. Biol Chem.2003,278:15565-15570.
[26]Brown MS, Goldstein JL. The SREBP pathway:regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor. [J]. Cell,1997, 89:331-340.
[27]Oram JF, Vaughan AM. ABCA1-mediated transport of cellular cholesterol and phospholipids to HDL apolipoproteins [J].Current Opinion in Lipidology.2000, 11:253-260.
[28].Brooks-Wilson A, Marcil M, Clee SM, et al. Mutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency. Nature Genet.1999,2 2:336-345.
[29].Lawn RM, Wade DP, Garvin MR, et al. The Tangier disease gene product ABC1 controls the cellular apolipoprotein-mediated lipid removal pathway. [J]. Clin Invest.1999,104:R25-R31.
[30]McNeish J, Aiello RJ, Guyot D, et al. High density lipoprotein deficiency and foam cell accumulation in mice with targeted disruption of ATP-binding cassette transporter-1.[J]. Proc.Natl.Acad.Sci.U.S.A.2000,97:4245-4250.
[31].Lee MH, Lu K, Hazard S, et al. Identification of a gene, ABCG5, important in the regulation of dietary cholesterol absorption. [J].Nature Genet.2001,27:79-83.
[32]Lu K, Lee MH, Hazard S, et al. Two genes that map to the STSL locus cause sitosterolemia:genomic structure and spectrum of mutations involving sterolin-1 and sterolin-2, encoded by ABCG5 and ABCG8, respectively.[J].Am J Hum Genet.2001,69:278-290.
[33]Repa JJ, Berge KE, Pomajzl C, et al. Regulation of ATP-binding cassette steroltransporters ABCG5 and ABCG8 by the liver X receptors alpha and beta. [J].Biol.Chem.2002,277:18793-18800.
[34]Mulligan JD, Flowers MT, Tebon A, et al.ABCAl is essential for efficient basolateral cholesterol efflux during the absorption of dietary cholesterol in chickens.[J].Biol Chem.2003,278:13356-13366.
[35]Field FJ, Born E, Mathur SN. LXR/RXR ligand activation enhances basolateral efflux of beta-sitosterol in CaCo-2 cells.[J].Lipid Res.2004,45:905-913.
[36]Repa JJ, Turley SD, Lobaccaro JA, et al. Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers [J]. Science.2000, 289:1524-1529.
[37]Peet DJ, Turley SD, Ma W, etal. Cholesterol and bile acid metabolism are impired in mice leaking the nuelear oxysterol receptor LXR alpher.1998, 93:693-704.
[38]Agellon LB, Drover VA, Cheema SK, et al. Dietary cholesterol fails to stimulate the human cholesterol 7alpha-hydroxylase gene(CYP7A1) in transgenic mice.[J]. Biol Chem.2002,277:20131-20134.
[39].Chen JY, Levy-Wilson B, Goodart S, et al. Mice expressing the human CYP7A1 gene in the mouse CYP7A1 knock-out background lack induction of CYP7A1 expression by cholesterol feeding and have increased hypercholesterolemia when fed a high fat diet. [J]. Biol Chem.2002,277:42588-42595.
[40]Repa JJ, Liang G, Ou J, et al. Regulation of mouse sterol regulatory element-binding protein-lc gene(SREBP-lc) by oxysterol receptors, LXRalpha and LXRbeta. Genes Dev,2000,14:2819-2830,
[41]Repa JJ. The Liver X receptor(LXR) and hepatic lipogenesis. The carbohydrate response element binding protein is a target gene of LXR. J Biol Chem,2007,282: 743-751.
[42]Zhou J, Febbraio M, Wada T, et al. Hepatic fatty acid transporter CD36 is a common target of LXR, PXR, and PPARgamma in promoting steatosis. Gast roenterology,2008,134:556-567.
[43]Beyea MM, Heslop CL, Sawyez CG, et al. Selective up-regulation of LXR regulated genes ABCA1, ABCG1, and apoE in macrophages through increased endogenous synthesis of 24(S),25-epoxycholesterol.J Biol Chem,2007,282: 5207-5216.
[44]Qninet E M, Savio D A, Halpern AR, et al. Liver X receptor(LXR)-beta regulation in LXRalpha-deficient mice:implications for therapeutic targeting. Mol Pharmacol,2006,70:1340-1349.
[45]Parks DJ, Blanchard SG, Bledsoe JK, et al. Bile acid:natural ligands for an orphan nuclear receptor. Science,1999,284:1365-1368.
[46]Rizzo G, Renga B, Mencarelli A, et al.Role of FXR in regulating bile acid homeostasis and relevance for human diseases. Curr Drug Targets Immune Endocr Metabol Disord.2005 Sep; 5(3):289-303
[47]Anisfeld A M, Kast Woelbern H R, Meyer M E, et al. Syndecan-1 expression is regulated in an isoform specific manner by the farnesoid X receptor[J]. Biol Chem, 2003,278(22):20420-20428.
[48]Watanabe M, Houten S M, Wang L, et al. Bile acids lower triglyceride levels via a pathway involving FXR, SHP and SREBP-lc[J]. J Clin Invest,2004,113(10): 1408-1418.
[49]Srivastava N.ATP-binding cassette transporter Al key roles in cellular lipid transport and atheroselerosis. Mol Cell Biochem,2002,237:155-164
[50].Oram J F, Lawn R M. ABCAI:the gate keeper for eliminating excess tissue cholesterol. J Lipid Res,2001,42:1173-1179、
[51]Clee SM, Zwinderman AH, Engert JC, et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease[J]. Circulation,2001,103:198-205.
[52]Tang CK, Yi GH, Yang JH, et al. Oxidized LDL upregulated ATP binding cassette transporter-1 in T'HP-1 macrophages[J]. Acta Pharmaeol Sin,2004,25(5): 581-586.
[53]de Vogel-van den Bosch, H. M. et al. A cholesterol-free, high-fat diet suppresses gene expression of cholesterol transporters in murine small intestine. Am J Physiol Gastrointest Liver Physiol 2008,294:1171-1180
[54]Francis,GA., Knopp, R.H. Oram,J.F. Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease.J.Clin. Invest, 1995,96:78-87
[2]杨诗杰,苏汝好,项岚等,降血脂药的应用现状及研究进展,医药论坛杂志,2006,27(1)：90-92
[3]Kajinami K, Takekoshi N. Cholesterol absorption inhibitors in development as potential therapeutics. Expert Opin Investig Drugs,2002,21 (3):831-835.
[4]Mann, G. V., Spoerry, A., Gray, M.& Jarashow, D. Atherosclerosis in the Masai. Am J Epidemiol,1972,95:26-37.
[5]Lin DC.Probiotics as functional foods.Nutr Clin Pract.2003,8(6):497-506.
[6]Larkin TA, Astheimer LB, Price WE.Dietary combination of soy with a probiotic or prebiotic food significantly reduces total and LDL cholesterol in mildly hypercholesterolaemic subjects.Eur J Clin Nutr.2007 Oct 17:236-239
[7].韩俊华,盛晓甘.乳酸菌降胆固醇作用的现状,中国乳品工业,2002,30(3)：16-20。
[8]Jaspers.D.A.Linda K.M, Lloyd.D.L.Effect of consuming yogurts prepared with three culture strains on human serum lipoproteins.Journal Food Science,1984,49:1178-1181.
[9]郑坚.乳酸菌对血脂的影响.黄冈师范学院学报,2002,22(3)：37-53
[10]Pereira.D.I. Gibson.GR. Effects of consumption of probiotics and prebiotics on serum lipid level in humans. Crit Rev Biochem Mol Biol,2002,37 (4):259-281.
[11]Gilliland.S.E, Nelson.C.R and Maxwel L C. Assilation of cholesterol by Lactobacillus acidophilus. Appl. Envi Micr,1985,49:377-381
[12]Buck.L.M, Gilliland.S.E. Comparisons of freshly isolated strains of Lactobacillus acidophilus of human intestinal origin for ability to assimilate cholesterol during growth.J Dairy Sci,1994,77:2925-2933.
[13]Dambekodi P.C. Gilliland S.E. Incorporation of cholesterol into the cellula membrane of bifidobacterium longurn. J dairy Sci.1998,81:1818-1824
[14]Don.D.O, Kim S.H, Gilliland S.E. Incorporation of cholesterol into the cell membrane of Lactobacillus acidophilus ATCC 43121.J Dairy Sci,1997,80: 3107-3113.
[15]Thome K.D. Barker.D.C.The occurrence of bactoprenol in the mesosome and plasma membranes of Lactobacillus casei and Lactobacillus plantarum.J Gen Microbiol,1972,70:87
[16]Zhao JR, Yang H.Progress in the effect of probiotics on cholesterol and its mechanism.Wei Sheng Wu Xue Bao.2005,45(2):315-319.
[17]Pereira DI, McCartney AL, Gibson GR.An in vitro study of the probiotic potential of a bile-salt-hydrolyzing Lactobacillus fermentum strain, and determination of its cholesterol-lowering properties. Appl Environ Microbiol.2003,69(8):4743-52.
[18]Buck L M, Gilliland S E. Comparisons of freshly isolated strans of lactobacillus Acidophilus of human in testinal origin for ability to assimilate cholesterol during growth..J Dairy Sei,1994,77:2925-2933
[19]Mott G E. Lowering of serum cholesterol by intestinal bacteria in cholesterol-fed piglets. Lipids,1993(8):428
[20]Tarant M P, Seama F. Bile salt hydrolase plays a key role on cholesterol removal by Lactobacillus reuteri. Biotechnol Lett,1997,19:845-47
[21]Dilmi-Bouras A.Assimilation (in vitro) of cholesterol by yogurt bacteria. Ann Agric Environ Med.2006,13(1):49-53.
[22]Grill JP, Cayuela C, Antoine JM, et al.Effects of Lactobacillus amylovorus and Bifidobacteria breve on cholesterol. Lett Appl Microbiol.,2000, Aug:31(2):154-156.
[23]Park YH, Kim JG, Shin YW,et al. Effect of dietary inclusion of Lactobacillus acidophilus ATCC 43121 on cholesterol metabolism in rats.J Microbiol Biotechnol. 2007,17(4):655-662.
[24]Han KH, Iijuka M, Shimada K, et al. Adzuki resistant starch lowered serum cholesterol and hepatic 3-hydroxy-3-methylglutaryl-CoA mRNA levels and increased hepatic LDL-receptor and cholesterol 7alpha-hydroxylase mRNA levels in rats fed a cholesterol diet.Br J Nutr,2005,94(6):902-908.
[25]Shima T, Fukushima K, Setoyama H,et al. Differential effects of two probiotic strains with different bacteriological properties on intestinal gene expression, with special reference to indigenous bacteria.FEMS Immunol Med Microbiol, 2008,52(1):69-77.
[26]Clee SM, Zwinderman AH, Engert JC, et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease[J]. Circulation,2001,103 (1):198-205
[27]Tang CK, Yi GH, Yang JH, et al. Oxidized LDL upregulated ATP binding cassette transporter-1 in T'HP-1 macrophages[J]. Acta Pharmaeol Sin,2004; 25(5): 581-586.
[28]Feng B. Tabas I. ABCA 1-mediated cholesterol efflux is defectivein free cholesterol-loaded maerophages. Mechanism involves enhanced ABCA 1 degradation in a process requiring full NPC1 activity. J Biol Chem,2002,277 (45):43271-43280
[29]de Vogel-van den Bosch, H. M. et al. A cholesterol-free, high-fat diet suppresses gene expression of cholesterol transporters in murine small intestine. Am J Physiol Gastrointest Liver Physiol 2008,294,G1171-1180
[30]Schwart K, Lawn RM, Wade DP. ABC 1 gene expression and Apo-A1 mediated cholesterol sterol efflux are regulated by LXR. Biochem Biophys Res Commun, 2000.274(3):794-802
[31]Wade DP, Owen JS. Regulation of the cholesterol efflux geneABCA1. Lancet, 2001,357(9251):161-163
[32]Huuskonen J, Vishnu M, Pullinger CR, et al. Regulation of ATP-binding cassette transporter Al transcription by thyroidhormone receptor. Biochemistry,2004,43 (6): 1626-1632
[33]Luo Y, Tall AR. Sterol upregulation of human CETP expressionin vitro and in transgenic mice by an LXR element. J Clin Invest,2000,105(4):513-520
[34]Francis G.A, Knopp R.H. Oram J.F. Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease.J.Clin.Invest.1995,96:78-87
[35]Lee MH, Lu K, Hazard S, et al.Identification of a gene, ABCG5, important in the regulation of dietary cholesterol absorption. Nat Genet,2001,27 (1):79-83.
[36]Lu k, Lee MH, Hazard S, et al. Two genes that map to the STSL locus cause sitosterolemia:genomic structure and spectrum of mutations involving sterolin-1 and sterolin-2, encoded by ABCG5 and ABCG8, respectively. Am J Hum Genet,2001,69 (2):278-290
[37]Berge KE, Tian H, Graf GA, et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters. Science,2000,290 (5497):1771-1775.
[38]Yu L, Li-Hawkins J, Hammer RE, et al. Overexpression of ABCG5 and ABCG8 promotes biliary cholesterol secretion and reduces fractional absorption of dietary cholesterol. J Clin Invest,2002,110 (5):671-680.
[39]Yu L, Hammer RE, Li-Hawkins J, et al. Disruption of Abcg5 and Abcg8 in mice reveals their crucial role in biliary cholesterol secretion. Proc Natl Acad Sci USA, 2002,99(25):16237-16242.
[40]Yu L, Gupta S, Xu F, et al. Expression of ABCG5 and ABCG8 is required for regulation of biliary cholesterol secretion. J Biol Chem,2005,280 (10):8742-8747.
[41]Duan LP, Wang HH, Wang DQ. Cholesterol absorption is mainlyregulated by the jejunal and ileal ATP-binding cassette sterol efflux transporters Abcg5 and Abcg8 in mice. J Lipid Res,2004,45 (7):1312-1323.
[42]Yu L, York J, von Bergmann K, et al. Stimulation of cholesterol excretion by the liver X receptor agonist requires ATP-binding cassette transporters G5 and G8. J Biol Chem,2003,278 (18):15565-15570.
[43]Repa JJ, Berge KE, Pomajzl C, et al. Regulation of ATP-bindingcassette sterol transporters ABCG5 and ABCG8 by the liver X receptors αand β. J Biol Chem,2002, 277(21):18793-18800.
[44]Shulman AI, Mangelsdorf DJ. Retinoid X receptor heterodimers in the metabolic syndrome. N Engl J Med,2005,353:604-615.
[44.1]赵瑞香,孙俊良,李明静,等.嗜酸乳杆菌同化MRS培养金中胆固醇能力的研究.中国微生态杂志,2005,17(4)：254-255
[45]刘丽莉,董铁有,杨协力.6种乳酸菌降胆固醇的体外实验.河南科技大学学报(自然科学版),2005,26(6)：85-88
[46]Reddy, K. B., Raghavendra, P., Kumar, B. G., et al. Screening of probiotic properties of lactic acid bacteria isolated from Kanjika, an ayruvedic lactic acid fermented product:an in-vitro evaluation. J Gen Appl Microbiol,2007,53,207-213
[47]香卫钦,于舒宁,张耀林,等.一株能降解胆固醇的乳酸菌的选育.生物技术,2001,11(05)：9-10
[48]肖琳琳,董明盛.西藏干酪乳酸菌降胆固醇特性研究.食品科学,2003,24(10)：142-145
[49]Gerard, P. Lepercq, P. Leclerc M, et al. Bacteroides sp. strain D8, the first cholesterol-reducing bacterium isolated from human feces. Appl Environ Microbiol 2007,73:5742-5749
[50]Mariat, D. The Firmicutes/Bacteroidetes ratio of the human microbiota changes with age. BMC Microbiol 2009,9:123,1471-2180
[51]Pfeiler EA, Klaenhammer TR.The genomics of lactic acid bacteria.Trends Microbiol,2007,15(12):546-553.
[52]Ljungh A, Wadstrom T.Lactic acid bacteria as probiotics. Curr Issues Intest Microbiol,2006,7(2):73-89.
[53]Ganzle MG, Vermeulen N, Vogel RF.Carbohydrate, peptide and lipid metabolism of lactic acid bacteria in sourdough. Food Microbiol,2007,24(2):128-138.
[54]Furzikova, T. M., Sorokulova, I. B., Serhiichuk, M. H., et al.The effect of antibiotic preparations and their combinations with probiotics on the intestinal microflora of mice. Mikrobiol Z,2000,62:26-35.
[55]Tannock, G. W., Tangerman, A., Van Schaik, A.et al. Deconjugation of bile acids by lactobacilli in the mouse small bowel. Appl Environ Microbiol,1994,60, 3419-3420.
[56]Pereira, D. I. Gibson, G. R. Cholesterol assimilation by lactic acid bacteria and bifidobacteria isolated from the human gut. Appl Environ Microbiol,2002,68, 4689-4693
[57]Klaver, F. A.& van der Meer, R. The assumed assimilation of cholesterol by Lactobacilli and Bifidobacterium bifidum is due to their bile salt-deconjugating activity. Appl Environ Microbiol,1993,59,1120-1124.
[58]Brashears MM, Gilliland SE, Buck LM.Bile salt deconjugation and cholesterol removal from media by Lactobacillus casei. J Dairy Sci.1998,81(8):2103-2110.
[59]郑建仙.功能性食品.第三卷.北京,中国轻工业出版社,2001：275-289
[60]徐叔云,卞如濂,陈修.药理实验方法学[M].第3版.北京：人民卫生出版社,2003,189-190
[61]Lin, C. Y., Tsai, C. Y. Lin, S. H. Effects of soy components on blood and liver lipids in rats fed high-cholesterol diets. World J Gastroenterol,2005,11:5549-5552
[62]Lepercq P, Relano P, Cayuela C, et al. Bifidobacteria animalis strain DN-173 010 hydrolyses bile salts in the gastrointestinal tract of pigs. Scand J Gastroenterol.2004, 39(12):1266-1271.
[63]石如玲,赵朝贤,朱海暴,等。大鼠胆汁酸合成加强时肝脏双功能蛋白mRNA表达及活性升高.基础医学与临床,2006,26(7)：720-723
[64]Kajiura K, Ohkusa T, Okayasu I. Relationship between fecal bile acids and the occurrence of colorectal neoplasia in experimental murine ulcerative colitis.Digestion. 1998; 59 (1):69-72.
[65]申瑞玲,董吉林,李文全.燕麦p-葡聚糖对高脂血症大鼠胆固醇代谢的影响.中国食品学报,2009,9(3)：14-19
[66]Fukada Y, Kimura K,Ayaki Y.Effect of chitosan feeding on intestinal bile acid metabolism in rats[J].Lipids,1991:395-399
[67]薛琨,郭红卫,陈凤麟,中链脂肪酸对营养性肥胖大鼠体重及脂质代谢的作用,卫生研究,2006,35(2)：187-190
[68]Moghadasian, M. H., Frohlich, J. J. McManus, B. M. Advances in experimental dyslipidemia and atherosclerosis. Lab Invest,2001,81:1173-1183
[69]陈凯,张雁芳,王倩,等.高胆固醇饲养兔鹤鹑和大鼠诱发高血脂和动脉粥样硬化的特征.解放军药学学报,2001,117-124.
[70]Boehler, N. et al. Antilithiasic effect of beta-cyclodextrin in LPN hamster: comparison with cholestyramine. J Lipid Res,1999,40:726-734
[71]Osono, Y., Woollett, L. A., Herz, J.& Dietschy, J. M. Role of the low density lipoprotein receptor in the flux of cholesterol through the plasma and across the tissues of the mouse. J Clin Invest,1995,95:1124-1132
[72]Spady, D. K.& Cuthbert, J. A. Regulation of hepatic sterol metabolism in the rat. Parallel regulation of activity and mRNA for 7 alpha-hydroxylase but not 3-hydroxy-3-methylglutaryl-coenzyme A reductase or low density lipoprotein receptor. J Biol Chem,1992,267:5584-5591
[73]Bhathena, J., Martoni C., Kulamarva, A., et al. Orally delivered microencapsulated live probiotic formulation lowers serum lipids in hypercholesterolemic hamsters. J Med Food,2009,12(2):310-319.
[74]Kim, N. H., Moon. P. D., Kim, S. J, et al. Lipid profile lowering effect of Soypro fermented with lactic acid bacteria isolated from Kimchi in high-fat diet-induced obese rats. Biofactors,2008,33(1):49-60.
[75]Fukushima, M.& Nakano, M. Effects of a mixture of organisms, Lactobacillus acidophilus or Streptococcus faecalis on cholesterol metabolism in rats fed on a fat-and cholesterol-enriched diet. Br J Nutr,1996,76:857-867
[76]Keim N L, Marlett J A, Amundsopn C H. The cholesterolemic effect of skim milk in young men consuming controlled diets[J].Nutrition research,1981, 1:422-429.
[77]Rossouw, J. E., Burger, E. M., Van der Vyver, P. et al.The effect of skim milk, yoghurt, and full cream milk on human serum lipids. Am J Clin Nutr,1981,34: 351-356.
[78]Hashimoto H, Yamazaid K, He F, et al. Hypocholesterolemic effects of Lactobacillus casei subsp. casei TMC 0409 strain observed in rats fed cholesterol contained diets[J].Animal Science Journal,1999,72:90-97.
[79]任邦哲等.生物化学与临床医学.长沙,湖南科学技术出版社,1992：202-206
[80]Nomiyama T.Bruemmer D. Liver X receptors as therapeutic targets in metabolism and atherosclerosis. Curr Atheroscler Rep,2008,10:88-95.
[81]Clee SM, Zwinderman AH, Engert JC, et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease[J]. Circulation,2001,103(1):198-205.
[82]Tang CK, Yi GH, Yang JH, et al. Oxidized LDL upregulated ATP binding cassette transporter-1 in T'HP-1 macrophages[J]. Acta Pharmaeol Sin,2004; 25(5): 581-6.
[83]Francis,GA.,Knopp,R.H. Oram,J.F. Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease.J.Clin.Invest.1995,96:78-87
[84]Repa, J. J., Turley, S. D., Laboccaro, J.-M.A., et al. Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers. Science (Washington, DC) 2000,289:1524-1529.
[85]Berge, K. E., Tian, H., Graf, G. A., et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters.Science (Washington, DC),2000,290:1771-1775.
[86]Osono, Y., Woollett, L. A., Herz, J.& Dietschy, J. M. Role of the low density lipoprotein receptor in the flux of cholesterol through the plasma and across the tissues of the mouse. J Clin Invest,1995,95:1124-1132
[87]Spady, D. K.& Cuthbert, J. A. Regulation of hepatic sterol metabolism in the rat. Parallel regulation of activity and mRNA for 7 alpha-hydroxylase but not 3-hydroxy-3-methylglutaryl-coenzyme A reductase or low density lipoprotein receptor. J Biol Chem,1992,267:5584-5591.
[88]Costet, P., Luo, Y., Wang, N. et al. Sterol-dependent transactivation of the ABC1 promoter by the liver X receptor/retinoid X receptor.J. Biol Chem,2000,275: 28240-28245.
[89]Edwards PA. Kast HR, Anisfeld AM, et al.The adoption of LXR and FXR and their roles in lipid homeostasis J Lipid Res,2002,43(1):2-12.
[90]Repa, J. J., Dietschy, J. M. Turley, S. D.et al. Inhibition of cholesterol absorption by SCH 58053 in the mouse is not mediated via changes in the expression of mRNA for ABCA1, ABCG5, or ABCG8 in the enterocyte. J. Lipid Res.2002,43:1864-1874.
[91]Repa, J.J, Liang G, Ou J, et al. Regulation of mouse sterol regulatory element-binding protein-lc gene (SREBP-1c) by oxysterol receptors, LXRa and LXRp. Genes Dev,2000,14:2819-2830.
[1]任邦哲等.生物化学与临床医学.长沙,湖南科学技术出版社,1992：202-206
[2]Peet DJ, lanowski BA, Mangelsdorf DI.111e LXRs:a new class of oxysterol receptors. Curr Opin Genet Dev 1998; 8:571-575
[3]Willy, P. J. et al. LXR, a nuclear receptor that defines a distinct retinoid response pathway. Genes Dev 9,1033-1045 (1995).
[4]Bjorkhem I, Diczfalusy U.24(S),25-Epoxycholesterol-A Potential Friend.[J].Arteriosclerosis,Thrombosis&Vascular Biology.2004,24(12):2209-2210.
[5]Rowe AH, Argmann CA, Edwards JY,et al. Enhanced synthesis of the oxysterol 24(S),25-epoxycholesterol on macrophages by inhibitors of 2, 3-oxidosqualene:lanosterol cyclase.[J].Circulation Research.2003,93:717-725.
[6]Fu X, Menke JG, Chen Y, et al.27-hydroxycholesterol is an endogenous ligand for liver X receptor in cholesterol-loaded cells.[J].Biol.Chem.2001,276:38378-38387.
[7]Colombo J, Kannass KN, Shaddy DJ, et al. Maternal DHA and the development of attention in infancy and toddlerhood. Child Dev,2004,75(4):1254-1267
[8]Song C, Liao S.Cholestenoic acid is a naturally occurring ligand for liver X receptor alpha.[J].Endocrinology 2000,141:4180-4184.
[9]Sparrow CP,Baffic J,Lam MH,et al.A potent synthetic LXR agonist is more effectivethan cholesterol loading at inducing ABCA1 mRNA and stimulating cholesterol efflux.[J].Biol.Chem.2002,277:10021-10027.
[10]Joseph SB, McKilligin E, Pei L,et al. Synthetic LXR ligand inhibits the development of atherosclerosis in mice.[J].Proc.Natl.Acad.Sci.U.S.A,2002, 99:7604-7609.
[11].Song C,Hiipakka RA,Liao S.Selective activation of liver X receptor alpha by6alpha-hydroxy bile acids and analogs.[J].Steroids.2000,65:423-427.
[12]Janowski BA,Grogan MJ,Jones SA,et al.Structural requirements of ligands for the oxysterol liver X receptors LXRalpha and LXRbeta [J]. Proc.Natl.Acad.Sci.U.S.A.1999,96:266-271.
[13]Zelcer N, Tontonoz P. Liver X receptors as integrators of metabolic and inflammatory signaling. J Clin Invest,2006,116:607-614
[14]Geyeregger R, Zeyda M, Stulnig TM, et al. Liver X receptors in cardiovascular and metabolic disease. Cell Mol Life Sci,2006:63:524-539
[15]Shulman AI, Mangelsdorf DJ.Retinoid X receptor heterodimers in the metabolic syndrome. N Engl J Med,2005,353:604-615.
[16]Laffitte BA, Repa JJ, Joseph SB, et al. LXRs control lipid-inducible expression of apolipo-protein E gene in macrophages and adipose tissue. Proe Natl Acad Sci USA,2001,98:507-512.
[17]Ishimoto K Tachibana K, Sumitomo M, et al. Identification of human low-density lipoprotein receptor as a novel target gene regulated by liver X receptor alpha. FEBS Lett,2006,580:4929-4933
[18]Brown MS, Goldstein JL. The SREBP pathway:regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor [J].Cell,1997, 89:331-340.
[19]Horton JD, Goldstein JL, Brown MS. SREBPs:activators of the complete program of cholesterol and fatty acid synthesis in the liver [J]. Clin Invest.2002, 109:1125-1131.
[20]Peet DJ, Turley SD, Ma W, et al. Cholesterol and bile acid metabolism are impaired in mice lacking the nuclear oxysterol receptor LXR alpha.[J].Cell,1998, 93:693-704.
[21]Alberti S, Schuster GU, Parini P, et al. Hepatic cholesterol metabolism and resistance to dietary cholesterol in LXRbeta-deficient mice.[J].Clin.Invest.2001, 107:565-573.
[22]Schultz JR, Tu H, Luk A, et al. Role of LXRs in control of lipogenesis [J].Genes Dev.2000,14:2831-2838.
[23]Song C, Hiipakka RA, Liao S. Auto-oxidized cholesterol sulfates are antagonistic ligands of liver X receptors:implications for the development and treatment of atherosclerosis.[J].Steroids.2001,66:473-479.
[24]Berge KE, Tian H, Graf GA, et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters. [J]. Science,2000, 90:1771-1775.
[25]Yu L, York J, von Bergmann K, et al. Stimulation of cholesterol excretion by the liver X receptor agonist requires ATP-binding cassette transporters G5 and G8. [J]. Biol Chem.2003,278:15565-15570.
[26]Brown MS, Goldstein JL. The SREBP pathway:regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor. [J]. Cell,1997, 89:331-340.
[27]Oram JF, Vaughan AM. ABCA1-mediated transport of cellular cholesterol and phospholipids to HDL apolipoproteins [J].Current Opinion in Lipidology.2000, 11:253-260.
[28].Brooks-Wilson A, Marcil M, Clee SM, et al. Mutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency. Nature Genet.1999,2 2:336-345.
[29].Lawn RM, Wade DP, Garvin MR, et al. The Tangier disease gene product ABC1 controls the cellular apolipoprotein-mediated lipid removal pathway. [J]. Clin Invest.1999,104:R25-R31.
[30]McNeish J, Aiello RJ, Guyot D, et al. High density lipoprotein deficiency and foam cell accumulation in mice with targeted disruption of ATP-binding cassette transporter-1.[J]. Proc.Natl.Acad.Sci.U.S.A.2000,97:4245-4250.
[31].Lee MH, Lu K, Hazard S, et al. Identification of a gene, ABCG5, important in the regulation of dietary cholesterol absorption. [J].Nature Genet.2001,27:79-83.
[32]Lu K, Lee MH, Hazard S, et al. Two genes that map to the STSL locus cause sitosterolemia:genomic structure and spectrum of mutations involving sterolin-1 and sterolin-2, encoded by ABCG5 and ABCG8, respectively.[J].Am J Hum Genet.2001,69:278-290.
[33]Repa JJ, Berge KE, Pomajzl C, et al. Regulation of ATP-binding cassette steroltransporters ABCG5 and ABCG8 by the liver X receptors alpha and beta. [J].Biol.Chem.2002,277:18793-18800.
[34]Mulligan JD, Flowers MT, Tebon A, et al.ABCAl is essential for efficient basolateral cholesterol efflux during the absorption of dietary cholesterol in chickens.[J].Biol Chem.2003,278:13356-13366.
[35]Field FJ, Born E, Mathur SN. LXR/RXR ligand activation enhances basolateral efflux of beta-sitosterol in CaCo-2 cells.[J].Lipid Res.2004,45:905-913.
[36]Repa JJ, Turley SD, Lobaccaro JA, et al. Regulation of absorption and ABC1-mediated efflux of cholesterol by RXR heterodimers [J]. Science.2000, 289:1524-1529.
[37]Peet DJ, Turley SD, Ma W, etal. Cholesterol and bile acid metabolism are impired in mice leaking the nuelear oxysterol receptor LXR alpher.1998, 93:693-704.
[38]Agellon LB, Drover VA, Cheema SK, et al. Dietary cholesterol fails to stimulate the human cholesterol 7alpha-hydroxylase gene(CYP7A1) in transgenic mice.[J]. Biol Chem.2002,277:20131-20134.
[39].Chen JY, Levy-Wilson B, Goodart S, et al. Mice expressing the human CYP7A1 gene in the mouse CYP7A1 knock-out background lack induction of CYP7A1 expression by cholesterol feeding and have increased hypercholesterolemia when fed a high fat diet. [J]. Biol Chem.2002,277:42588-42595.
[40]Repa JJ, Liang G, Ou J, et al. Regulation of mouse sterol regulatory element-binding protein-lc gene(SREBP-lc) by oxysterol receptors, LXRalpha and LXRbeta. Genes Dev,2000,14:2819-2830,
[41]Repa JJ. The Liver X receptor(LXR) and hepatic lipogenesis. The carbohydrate response element binding protein is a target gene of LXR. J Biol Chem,2007,282: 743-751.
[42]Zhou J, Febbraio M, Wada T, et al. Hepatic fatty acid transporter CD36 is a common target of LXR, PXR, and PPARgamma in promoting steatosis. Gast roenterology,2008,134:556-567.
[43]Beyea MM, Heslop CL, Sawyez CG, et al. Selective up-regulation of LXR regulated genes ABCA1, ABCG1, and apoE in macrophages through increased endogenous synthesis of 24(S),25-epoxycholesterol.J Biol Chem,2007,282: 5207-5216.
[44]Qninet E M, Savio D A, Halpern AR, et al. Liver X receptor(LXR)-beta regulation in LXRalpha-deficient mice:implications for therapeutic targeting. Mol Pharmacol,2006,70:1340-1349.
[45]Parks DJ, Blanchard SG, Bledsoe JK, et al. Bile acid:natural ligands for an orphan nuclear receptor. Science,1999,284:1365-1368.
[46]Rizzo G, Renga B, Mencarelli A, et al.Role of FXR in regulating bile acid homeostasis and relevance for human diseases. Curr Drug Targets Immune Endocr Metabol Disord.2005 Sep; 5(3):289-303
[47]Anisfeld A M, Kast Woelbern H R, Meyer M E, et al. Syndecan-1 expression is regulated in an isoform specific manner by the farnesoid X receptor[J]. Biol Chem, 2003,278(22):20420-20428.
[48]Watanabe M, Houten S M, Wang L, et al. Bile acids lower triglyceride levels via a pathway involving FXR, SHP and SREBP-lc[J]. J Clin Invest,2004,113(10): 1408-1418.
[49]Srivastava N.ATP-binding cassette transporter Al key roles in cellular lipid transport and atheroselerosis. Mol Cell Biochem,2002,237:155-164
[50].Oram J F, Lawn R M. ABCAI:the gate keeper for eliminating excess tissue cholesterol. J Lipid Res,2001,42:1173-1179、
[51]Clee SM, Zwinderman AH, Engert JC, et al. Common genetic variation in ABCA1 is associated with altered lipoprotein levels and a modified risk for coronary artery disease[J]. Circulation,2001,103:198-205.
[52]Tang CK, Yi GH, Yang JH, et al. Oxidized LDL upregulated ATP binding cassette transporter-1 in T'HP-1 macrophages[J]. Acta Pharmaeol Sin,2004,25(5): 581-586.
[53]de Vogel-van den Bosch, H. M. et al. A cholesterol-free, high-fat diet suppresses gene expression of cholesterol transporters in murine small intestine. Am J Physiol Gastrointest Liver Physiol 2008,294:1171-1180
[54]Francis,GA., Knopp, R.H. Oram,J.F. Defective removal of cellular cholesterol and phospholipids by apolipoprotein A-I in Tangier Disease.J.Clin. Invest, 1995,96:78-87