胆汁酸代谢

胆汁酸是胆汁中存在的一类胆烷酸的总称,以钠盐或钾盐的形式存在,是胆汁的主要有机成分。胆汁酸在肝细胞内由胆固醇转化而来,为脂类物质(包括脂溶性维,卜素)的消化、吸收所必需。     

胆汁酸代谢途径的研究进展

肝脏的胆汁酸代谢在维持机体的胆固醇稳态中起了重要的作用。本对胆汁酸代谢的两条途径和它们在整个胆汁酸代谢中的相应地位及与胆汁酸代谢紊乱相关的两种疾病作一综述。     

胆汁酸代谢途径的研究进展

肝脏的胆汁酸代谢在维持机体的胆固醇稳态中起了重要的作用。本文对胆汁酸代谢的两条途径和它们在整个胆汁酸代谢中的相应地位及与胆汁酸代谢紊乱相关的两种疾病作一综述。     

人肝细胞安定代谢功能的测定方法

药物代谢是肝细胞的重要生物功能之一[1,2].通过测定肝细胞培养液中某一物质的浓度变化,可准确反映肝细胞代谢功能[3-5],而国内尚无这方面报道.为此我们参照国外人工肝研究经验[1,5,6],选择安定为指标,通过研究,找到一种培养人肝细胞药物代谢功能的测定方法.     

亚低温培养对猪肝细胞形态与功能的影响

目的 评价亚低温培养对猪肝细胞形态与功能的影响,探讨亚低温保存和运输肝细胞的可行性.方法 将分离的新生猪肝细胞分别于25℃、28℃、33℃条件下培养24 h后,恢复至37℃继续培养,观察亚低温培养肝细胞的形态及LDH和AST漏出量,检测复温前后肝细胞白蛋白合成率、氨清除率和尿素合成率.结果 亚低温培养24 h和复温37...     

重型肝炎患者血浆对体外培养猪肝细胞的影响

有研究证实肝衰竭患者血浆或血清对体外培养的HepG2、HHY41细胞有毒性作用。现阶段生物人工肝临床研究的主要细胞材料为猪肝细胞，肝衰竭患者血浆对其毒性作用研究鲜见报道，因此研究旨在采用猪肝细胞，观察我国数量众多的慢性乙型病毒性重型肝炎患者血浆对其体外影响。     

肝衰竭患者血浆(血清)对体外培养肝细胞毒性作用的研究现状

生物人工肝是以培养肝细胞为基础的人工肝支持系统,高活性和功能良好的肝细胞是其基本要素之一,然而,由于肝衰竭患者肝脏大量肝细胞坏死,导致机体代谢紊乱和大量毒性物质堆集,这些毒性物质会对反应器中肝细胞产生毒性作用,直接影响生物人工肝的治疗效果.因此,了解肝衰竭患者血浆（liver failure plasma,LFP）或血清（liver failure serum,LFS）对体外培养肝细胞的各种不良作用,对生物人工肝的临床应用有重要意义.本文综述近年来在该领域的研究进展.     

生物人工肝之肝细胞分离和培养研究现状

组合型生物人工肝支持系统(Hybrid Bioartificial Liver Support System. HBLSS)具备解毒、分泌、合成与转化等功能。在国外已完成动物试验,并进入了Ⅰ期临床试验,取得良好效果。笔者拟就现代生物人工肝的基础——肝细胞的分离和培养研究作一综述。 1 肝细胞来源 生物人工肝(BLSS)的肝细胞,要求既要有足够的数量,又要有完备的生物学活性。肝细胞来源大概有3条途径:①来自人或动物的肝脏分离的原代肝细胞;②肿瘤肝细胞建株后的     

混合生物人工肝细胞成分的初步研究：——乳猪肝细胞的分离 …

目的 为探讨乳猪肝细胞分离、体外培养的条件及其生长方式。方法 用两步灌注结合胶原酶消化法分离乳猪肝细胞,用激光条件培养基进行体外培养,ＥＤＴＡ消化传代,测定细胞的活性,观察其生长方式,群体倍增时间及蛋白质和ＤＮＡ的合成。结果 在 原酶浓度为０．０７５％,细胞的收获笔成活率较高,原代和传代的肝细胞生长良好,原代肝细胞倍增时间较短,ＤＮＡ和蛋白质的合成也较活跃,与传代细胞相比,无明显差别（Ｐ〉０．０５     

胆汁酸代谢改变对肝癌发生影响机制的研究

目的探讨胆汁酸(bile acids,BAs)各组分在乙型肝炎(乙肝)相关性肝细胞癌(hepatocellur carcinoma,HCC)患者血浆中的浓度及组成比例变化,进一步探索其与HCC的关系。方法用液相色谱-质谱联用手段分别检测24例HCC患者、15例乙肝肝硬化患者、6例慢性乙肝患者及12例健康对照者血浆中的各BAs组分的变化。用实时荧光定量PCR与免疫组织化学法检测15例肝癌组织与癌旁组织中IL-1β的表达水平。结果在24例HCC患者中,BAs组分胆酸、鹅脱氧胆酸、牛磺脱氧胆酸、石胆酸、甘氨鹅脱氧胆酸、甘氨脱氧胆酸相比乙肝肝硬化与健康对照组有明显升高,差异均有统计学意义(P均0.05),其中石胆酸浓度在不同临床分期患者中差异有统计学意义,C期明显高于B期和A期。癌组织中IL-1β的表达水平低于癌旁组织。结论血浆胆汁酸中石胆酸的浓度增高与肝癌进展相关,有可能成为HCC进展的评价指标。     

胆汁酸对糖脂代谢影响的研究现状

胆汁酸是胆汁的重要成分,主要在肝脏合成,在膳食脂肪的消化吸收和胆固醇的代谢调节中发挥重要作用.近年来研究发现,胆汁酸还可激活法尼酯X受体-α、TGK5等信号分子,通过多种信号途径反馈调节自身的肠肝循环,同时还有降低血浆高密度脂蛋白和甘油三酯的作用,并且还参与糖代谢的调节,与体内糖脂代谢的动态平衡密切相关.因此,一些胆汁酸相关的信号途径很有希望成为治疗代谢性疾病的新靶点.     

胆汁酸代谢与调控研究进展

胆汁酸是胆汁的主要成分,在肝细胞内由胆固醇转化而来,是肝脏清除胆固醇的主要方式。胆汁酸可促进脂类的消化和吸收,抑制胆汁中胆固醇的析出。胆汁酸的代谢包括合成、摄取转运、加工、排泄和肠肝循环等过程。上述过程的有序进行是保证体内胆汁酸正常代谢和机体稳态的基础,而体内对胆汁酸各个代谢过程的精细调控则是基础的保障。此文主要针对胆汁酸代谢调控进展,从分子和基因水平作一综述。     

Hepatotoxic bile acids increase cytosolic Ca++ activity of isolated rat hepatocytes

Effects of bile acids on cystolic Ca++ activity and cell viability of isolated rat hepatocytes were studied to test the hypothesis that bile acids may produce hepatotoxicity by increasing cystolic Ca++ activity. Changes in cystolic Ca++ activity were calculated from time-dependent changes in fluorescence of quin-2 loaded hepatocytes. Release of lactate dehydrogenase and changes in propodium iodide fluorescence were used to assess cell viability. Bile acids studied were unconjugated and taurine-conjugated cholate, chenodeoxycholate (and taurochenodeoxycholate), deoxycholate (and taurodeoxycholate) and lithocholate (and taurolithocholate). With the exception of cholate and taurocholate, bile acids increased cystolic Ca++ activity within 10 to 30 sec in a concentration-dependent fashion (0.05 to 1.0 mM) and in the order lithocholate = taurolithocholate greater than chenodeoxycholate = taurochenodeoxycholate = deoxycholate = taurodeoxycholate. The initial increase in cystolic Ca++ activity by bile acids was not due to cell damage, since bile acid-induced decreases in cell viability were not significant until 2 to 3 min. At higher concentrations of unconjugated bile acid, there was a secondary increase in quin-2 fluorescence corresponding temporally to the increase in propodium iodide fluorescence, indicating cell damage after the initial increase in cystolic Ca++ activity. The ability of conjugated and unconjugated bile acids to increase cystolic Ca++ activity was abolished and decreased (60 to 90%), respectively, in the absence of extracellular Ca++, indicating that extracellular Ca++ is the major source of the bile acid-induced increase in cystolic Ca++ activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of bile acids on hepatic protoporphyrin metabolism in perfused rat liver

To determine the effect of bile acids on hepatic protoporphyrin metabolism, balance studies were performed in isolated perfused rat livers. Hepatic protoporphyrin metabolism was found to increase linearly as a function of protoporphyrin dose in livers infused with and without taurocholate (0.7 mumol/min), but their rates differed significantly. Employing a standard 1500-nmol protoporphyrin bolus dose, infusions (0.7 mumol/min) of taurocholate, glycocholate, deoxycholate, and chenodeoxycholate, but not tauroursodeoxycholate or ursodeoxycholate, increased protoporphyrin metabolism 1.7- to 2.7-fold over control (0 bile acid) values. Bile acid infusion ranging from 0.175 to 1.4 mumol/min confirmed that both taurocholate and chenodeoxycholate increased protoporphyrin disposal significantly more than ursodeoxycholate. For all bile acids, the increase of protoporphyrin metabolism was most pronounced between biliary bile acid excretion rates of 10-50 nmol/min.g liver. These data indicate that (a) bile acids facilitated protoporphyrin metabolism, (b) bile acid structure influenced the effect, and (c) ursodeoxycholate may not be a prime candidate to study the role of bile acids in the treatment of protoporphyria.     

核受体在胆汁酸和胆固醇代谢中的作用

人体内多种核受体参与胆汁酸和胆固醇的代谢调节.近年来核受体调节胆汁酸及胆固醇代谢的研究已成为国内外研究的热点,其中尤以法尼酯X受体和肝X受体α作用最为重要,此文着重对该两种核受体的研究现状作一综述,对其他核受体作用作简要叙述.     

Abnormal metabolism of secondary bile acids in patients with cirrhosis

The composition of bile acids in human bile was determined in bile-rich duodenal fluid on four consecutive days in a group of seven patients with cirrhosis and eight control patients with no liver disease. There was a marked reduction of secondary biliary bile acids in cirrhotic patients. Possible mechanisms for these changes are discussed.     

Effects of calcisorb on fecal bile acids and fatty acids in human volunteers

The intake of calcium (Ca) is negatively associated with colorectal cancer (crc) risk. The aim of this study was to investigate in a double-blind, placebo-controlled trial, the effects of the Ca-binder Calcisorb, which is given to kidney stone patients with hypercalciuria type I, on risk factors for crc risk, bile acids (BA), and long-chain fatty acids (LCFA) in fecal water. Results show that the concentration of BA and LCFA in fecal water did not change, although the urinary excretion of Ca and magnesium (Mg) and the concentration of Ca and magnesium in fecal water decreased. The daily excretion of BA and LCFA acids decreased significantly (p < 0.05) during the Calcisorb period. In conclusion, binding dietary Ca and Mg with Calcisorb from a diet with a relatively low amount of fat does not enhance the solubility of BA and LCFA in fecal water.