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High level of deoxycholic acid in human bile does not promote cholesterol gallstone formation

World Journal of Gastroenterology 2003年第7期9卷 1576-1579页

作者： Ulf Gustafsson Staffan Sahlin curt einarsson Department of Surgery Danderyd HospitalStockholmSweden Division of Gastroenterology and Hepatology Department of MedicineHuddinge University HospitalKarolinska InstitutetStockholmSweden

AIM:To study whether patients with excess deoxycholic acid (DCA) differ from those with normal percentage of DCA with respect to biliary lipid composition and cholesterol saturation of gallbladder bile. METHODS:Bile was collected during operation through puncturing into the gallbladder from 122 cholesterol gallstone patients and 46 gallstone-free subjects undergoing *** data,biliary lipids,bile add composition, presence of crystals and nucleation time were analyzed. RESULTS:A subgroup of gallstone patients displayed a higher proportion of DCA in bile than gallstone free subjects. By choosing a cut-off level of the 90th percentile,a group of 13 gallstone patients with high DCA levels (mean 50 percent of total bile acids) and a large group of 109 patients with normal DCA levels (mean 21 percent of total bile acids) were *** mean age of the patients with high DCA levels was higher than that of the group with normal levels (mean age:62 years vs45 years) and so was the mean BMI (28.3 vs.24.7).Plasma levels of cholesterol and triglycerides were slightly higher in the DCA excess groups compared with those in the normal DCA *** was no difference in biliary lipid composition,cholesterol saturation,nucleation time or occurrence of cholesterol crystals in bile between patients with high and normal levels of DCA. CONCLUSION:Gallstone patients with excess DCA were of older age and had higher BMI than patients with normal *** two groups of patients did not differ with respect to biliary lipid composition,cholesterol saturation,nucleation time or occurrence of cholesterol *** is concluded that DCA in bile does not seem to contribute to gallstone formation in cholesterol gallstone patients.

关键词： Adolescent Adult Aged Aged, 80 and over Bile Body Mass Index Cholesterol Crystallization Deoxycholic Acid Female Gallstones Humans Lipids Male Middle Aged Research Support, Non-U.S. Gov't

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Gallbladder bile composition in patients with Crohn's disease

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World Journal of Gastroenterology 2006年第1期12卷 70-74页

作者： Annika Lapidus Jan-Erikkerlund curt einarsson Centre of Gastrointestinal Disease Ersta HospitalDepartment of SurgeryDanderyd Hospital and Department of Gastroenterology and HepatologyKarolinska Institutet at Karolinska University Hospital HuddingeStockholmSweden

AIM： To further elucidate the pathogenesis and mechanisms of the high risk of gallstone formation in Crohn＇s disease. METHODS： Gallbladder bile was obtained from patients with Crohn＇s disease who were admitted for elective surgery （27 with ileal/ileocolonic disease and 7 with Crohn＇s colitis）. Fourteen gallstone patients served as controls. Duodenal bile was obtained from ten healthy subjects before and after the treatment with ursodeoxycholic acid. Bile was analyzed for biliary lipids, bile acids, bilirubin, crystals, and crystal detection time （CDT）. Cholesterol saturation index was calculated. RESULTS： The biliary concentration of bilirubin was about 50% higher in patients with Crohn＇s disease than in patients with cholesterol gallstones. Ten of the patients with Crohn＇s disease involving ileum and three of those with Crohn＇s colitis had cholesterol saturated bile. Four patients with ileal disease and one of those with colonic disease displayed cholesterol crystals in their bile. About 1/3 of the patients with Crohn＇s disease had a short CDT. Treatment of healthy subjects with ursodeoxycholic acid did not increase the concentration of bilirubin in duodenal bile. Several patients with Crohn＇s disease, with or without ileal resection/disease had gallbladder bile supersaturated with cholesterol and short CDT and contained cholesterol crystals. The biliary concentration of bilirubin was also increased in patients with Crohn＇s colitis probably not due to bile acid malabsorption. CONCLUSION： Several factors may be of importance for the high risk of developing gallstones of both cholesterol and pigment types in patients with Crohn＇s *** skillful technical assistance of Ms Lisbet Benthin and Ms Ingela Arvidsson is acknowledged.

关键词： Bile acid Biliary lipid composition Bilirubin Crohn's disease Gallstone disease

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Bile acid formation in primary human hepatocytes

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World Journal of Gastroenterology 2000年第4期6卷 522-525页

作者： curt einarsson Ewa Ellis Anna Abrahamsson Bo-Gran Ericzon Ingemar Bjrkhem Magnus Axelson Division of Gastroenterology and Hepatology Department of Medicine Department of Transplantation Surgery Department of Clinical Chemistry Karolinska Institutet at Huddinge University Hospital StockholmSweden Department of Clinical Chemistry Karolinska Institutet at Karolinska Hospital StockholmSweden

AIM To evaluate a culture system for bile acidformation in primary human hepatocytes incomparison with HepG2 *** Hepatocytes were isolated fromnormal human liver tissue and were cultured inserum-free William’s E *** medium wascollected and renewed every 24 *** acids andtheir precursors in media were finally analysed bygas chromatography-mass *** Cholic acid(CA)andchenodeoxycholic acid(CDCA)conjugated withglycine or taurine accounted for 70% and 25% oftotal steroids.A third of CDCA was alsoconjugated with sulphuric *** thyroid hormone alone or in combination didnot significantly effect bile acid *** of cyclosporin A(10 μmol/L)inhibited thesynthesis of CA and CDCA by about 13% and30%,*** Isolated human hepatocytes inprimary culture behave as in the intact liver byconverting cholesterol to conjugated CA *** is in contrast to cultured HepG2 cells,which release large amounts of bile acidprecursors and unconjugated bile acids into themedium.

关键词： bile acid formation cell culture cholesterol metabolism cyclosporin human hepatocytes

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Analysis of ileal sodium/bile acid cotransporter and related nuclear receptor genes in a family with multiple cases of idiopathic bile acid malabsorption

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World Journal of Gastroenterology 2006年第47期12卷 7710-7714页

作者： Marco Montagnani Anna Abrahamsson Cecilia Glman Gsta Eggertsen Hanns-Ulrich Marschall Elisa Ravaioli curt einarsson Paul A Dawson Dipartimento di Medicina Interna e Gastroenterologia Università di Bologna Bologna Italy Center for Applied Biomedi-cal Research Università di Bologna Bologna Italy Center for Gastroenterology and Hepatology Karolinska University Hospital Huddinge Stockholm Sweden Center for Metabolism and Endocrinology Karolinska University Hospital Huddinge Stockholm Sweden Department of Laboratory Medicine Division of Clinical Chemistry Karolinska University Hospital Huddinge Stockholm Sweden Department of Internal Medicine Wake Forest University School of Medicine Winston-Salem NC 27157 United States

The etiology of most cases of idiopathic bile acid malabsorption （IBAH） is unknown. In this study, a Swedish family with bile acid malabsorption in three consecutive generations was screened for mutations in the ileal apical sodium-bile acid cotransporter gene （ASBT; gene symbol, SLC10A2） and in the genes for several of the nuclear receptors known to be important for ASBT expression： the farnesoid X receptor （FXR） and peroxisome proliferator activated receptor alpha （PPARα）. The patients presented with a clinical history of idiopathic chronic watery diarrhea, which was responsive to cholestyramine treatment and consistent with IBAH. Bile acid absorption was determined using ^75Se-homocholic acid taurine （SeHCAT）; bile acid synthesis was estimated by measuring the plasma levels of 7α-hydroxy-4-cholesten-3-one （C4）. The ASBT, FXR, and PPARα genes in the affected and unaffected family members were analyzed using single stranded conformation polymorphism （SSCP）, denaturing HPLC, and direct sequencing. No ASBT mutations were identified and the ASBT gene did not segregate with the bile acid malabsorption phenotype. Similarly, no mutations or polymorphisms were identified in the FXR or PPARα genes associated with the bile acid malabsorption phenotype. These studies indicate that the intestinal bile acid malabsorption in these patients cannot be attributed to defects in ASBT. In the absence of apparent ileal disease, alternative explanations such as accelerated transit through the small intestine may be responsible for the IBAM.

关键词： Bile acid malabsorption Diarrhea Genetics ^75Se-homocholic acid taurine test Nuclear receptors

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胆固醇结石病人肝脏脂质代谢异常的分子生物学研究

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外科理论与实践 2007年第5期12卷 414-421页

作者：蒋兆彦姜翀弋胡海所广军 Paolo Parini Gsta Eggertsen Matthew A Davis Lawrence L Rudel curt einarsson 韩天权张圣道上海交通大学医学院附属瑞金医院外科上海消化外科研究所上海东方医院外科 Division of Hepatology and Gastroenterology Department of MedicineKarolinska University Hospital Huddinge141 86 StockholmSweden Department of Pathology Section on Lipid SciencesWake Forest University School of MedicineWinston-SalemNorth Carolina27157

目的:研究导致胆石病人胆汁胆固醇过饱和的肝脏胆固醇和胆汁酸代谢途径中的分子生物学改变。方法:收集22例胆石病人和13例无胆石病的对照病人肝脏活检组织、胆囊胆汁和血浆。采用实时定量PCR检测肝脏基因表达,采用Western印迹法测定蛋... 详细信息

目的:研究导致胆石病人胆汁胆固醇过饱和的肝脏胆固醇和胆汁酸代谢途径中的分子生物学改变。方法:收集22例胆石病人和13例无胆石病的对照病人肝脏活检组织、胆囊胆汁和血浆。采用实时定量PCR检测肝脏基因表达,采用Western印迹法测定蛋白含量。结果:胆石病人较对照组ABCG5/ABCG8和LXRα基因的mRNA表达水平分别增加51%、59%和102%。肝脏SRBI的mRNA和蛋白含量均增加。结论:胆石病人ABCG5/ABCG8基因表达上调,可能与LXRα表达增加促进相关,这些异常是导致胆汁胆固醇过饱和的原因。此外,胆汁中过多的胆固醇可能来源于经肝脏高密度脂蛋白受体SRBI的摄取,而不是由于肝脏合成和酯化的异常。

关键词：胆固醇结石基因表达载脂蛋白类脂质累积病分子生物学

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胆固醇结石病人肝脏胆小管侧膜ATP基因表达差异的研究

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外科理论与实践 2005年第1期10卷 61-65页

作者：蒋兆彦韩天权所广军袁作彪姜志宏商俊蔡杏兴 Gsta Eggertsen curt einarsson 张圣道上海第二医科大学附属瑞金医院外科上海市东方医院外科 200120 瑞典斯德哥尔摩卡罗林斯卡医学院附属乌丁医院消化科

目的:本研究旨在测定比较胆石病人与对照组肝脏胆小管侧膜转运蛋白表达差异,以探讨胆石病发生的分子生物学机制。方法:研究包括20例胆囊胆固醇结石病人和11例无胆石症的对照。测定血清胆固醇和甘油三酯、胆汁胆固醇、胆汁酸和磷脂含量,... 详细信息

目的:本研究旨在测定比较胆石病人与对照组肝脏胆小管侧膜转运蛋白表达差异,以探讨胆石病发生的分子生物学机制。方法:研究包括20例胆囊胆固醇结石病人和11例无胆石症的对照。测定血清胆固醇和甘油三酯、胆汁胆固醇、胆汁酸和磷脂含量,采用Carey表计算胆汁胆固醇饱和指数。实时定量PCR法测定肝脏胆小管侧膜转运蛋白(ABCG5、ABCG8、ABCBll和ABCB4)mRNA的表达量。结果:胆石组血清胆固醇低于对照组(P<0.05)。胆石组胆汁胆固醇摩尔百分比和胆固醇饱和指数较对照组显著升高(P<0.01)。胆石组肝脏胆小管侧膜胆固醇转运蛋白ABCG5和ABCG8表达高于对照组,且后者差异具有统计学显著性(ABCG5:31.44±3.17Vs25.72±3.27,ABCG8:27.53±3.06vs17.81±2.23)。ABCBll和ABCB4表达在两组间差异无显著性。结论:本研究显示,胆石病主要病理生理异常为胆汁胆固醇过饱和,与肝脏胆小管侧膜胆固醇转运蛋白ABCG5和ABCG8的mRNA表达增加有关。

关键词：胆固醇结石基因表达载体蛋白质类

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