摘要
胆囊胆固醇结石病发病率有不断增加趋势。在胆石病发病机制中,胆汁胆固醇过饱和是胆石形成的必要条件。近年来的研究显示,胆石病患者肝肠循环脂质代谢异常是导致胆汁胆固醇过饱和的分子生物学基础:包括肝脏高密度脂蛋白受体增加胆固醇的摄人、胆小管侧膜胆固醇转运蛋白增加向胆汁中分泌以及经小肠摄人体内的胆固醇增加。大量实验证据表明,对肝肠循环脂质代谢异常进行有效干预,通过降低肝脏胆固醇负荷及其分泌,抑制小肠胆固醇摄取等多个环节,维持胆汁胆固醇的平衡,有望成为预防胆石形成的一系列新的措施。
Cholesterol gallstone disease is prevalent and its incidence is increasing in China. Supersaturation of biliary cholesterol is a prerequisite for gallstone formation. Recent studies show that disorders of hepatic-enteric metabolism of lipids play important roles in the pathogenesis of gallstone disease and these include: increased biliary cholesterol which originates from an increased uptake of plasma high density lipoprotein mediated by scavenger receptor B type 1, increased secretion of cholesterol into bile via hepatic canalicular cholesterol transporters, and increased intestinal cholesterol absorption in gallstone patients. These eventually lead to supersaturation of biliary cholesterol. Evidences also suggest that decreasing hepatic cholesterol loading, promoting biliary bile acids and phospholipids secretion, and/or inhibiting intestinal cholesterol absorption can moderate saturation of biliary cholesterol, and prevent gallstone formation.
出处
《中华肝胆外科杂志》
CAS
CSCD
北大核心
2011年第9期697-700,共4页
Chinese Journal of Hepatobiliary Surgery
基金
基金项目:国家自然科学基金(30672042,30700310)
上海市重点学科外科学基金(S30204)
瑞典Ruth Richard Julin Foundation.
关键词
胆固醇结石
发病机理
预防
Cholesterol gallstone
Pathogenesis Prevention