期刊文献+

胆汁酸的营养生理作用及代谢调控研究进展 被引量:15

Recent Progress in Nutrition Physiology Role and Metabolism Regulation of Bile Acids
下载PDF
导出
摘要 胆汁酸(BA)是由胆固醇在肝脏代谢产生的具有两性分子结构的化合物,对营养物质的消化吸收代谢和动物健康均有重要作用。一方面,BA通过其洗涤特性促进食物中脂类和脂溶性维生素的消化吸收,同时,BA还可以激活法尼醇X受体(FXR)、G蛋白偶联BA受体1(GPBAR1)和维生素D受体(VDR),从而在糖代谢、脂类代谢、免疫调节和BA稳态调节方面发挥重要作用;另一方面,由于高浓度的BA特别是疏水性强的BA表现出细胞毒性,妊娠期肝脏内胆汁淤积被认为是导致胎儿宫内发育迟缓、宫内窘迫症、早产甚至死亡的重要因素。本文简要介绍了BA的分类、BA的营养生理功能、BA稳态及营养对BA稳态的调节,以期为动物营养研究及动物生产调控提供新的视觉和参考。 Bile acids(BA)are amphipathic structure compound derived from the catabolism of cholesterol in liver.BA play an important role in digestion,absorption and metabolism of nutrients and maintenance of health.On one hand,BA can facilitate the solubilization,digestion and absorption of dietary lipids and fat-soluble vitamins owing to its detergent characteristics and regulate glucose metabolism,lipid metabolism,immunity adjustment and BA homeostasis through activating farnesoid X receptor(FXR),G protein-coupled bile acid receptor 1(GPBAR1)and vitamin D receptor(VDR).On the other hand,high concentration of BA showing cytotoxicity,intrahepatic cholestasis of pregnancy has been strongly implicated in fetal intrauterine growth retardation,intrauterine distress,premature and even death.This review briefly introduces the classification of BA,the nutritional and physiological functions of BA,BA homeostasis and its regulation through nutrition,which may provide new version and reference for animal nutrition and animal production.
作者 王朋 林森 吴德 方正锋 WANG Peng;LIN Sen;WU De;FANG Zhengfeng(Key Laboratory for Animal Disease Resistance Nutrition of the Ministry of Education,Animal Nutrition Institute,Sichuan Agricultural University,Chengdu 611130,China)
出处 《动物营养学报》 CAS CSCD 北大核心 2019年第5期2002-2011,共10页 CHINESE JOURNAL OF ANIMAL NUTRITION
基金 国家自然科学基金项目(31472109) 四川农业大学杰青后备人选培养基金项目(00924104) 四川铁骑力士校企合作项目(009H0405)
关键词 胆汁酸 糖代谢 脂代谢 胎儿存活 胆汁酸稳态 营养 bile acids glucose metabolism lipid metabolism fetal survival bile acid homeostasis nutrition
  • 相关文献

参考文献1

二级参考文献36

  • 1Baumgart DC,Dignass AU.Intestinal barrier function.Curr Opin Clin Nutr Metab Care 2002; 5:685-694.
  • 2Dehghan A,van Hoek M,Sijbrands EJ,Stijnen T,Hofman A,Witteman JC.Risk of type 2 diabetes attributable to C-reactive protein and other risk factors.Diabetes Care 2007; 30: 2695-2699.
  • 3Engstr m G,Hedblad B,Tydén P,Lindg rde F.Inflammation-sensitive plasma proteins are associated with increased incidence of heart failure:a population-based cohort study. Atherosclerosis 2009; 202:617-622.
  • 4Arrieta MC,Bistritz L,Meddings JB.Alterations in intestinal permeability.Gut 2006; 55:1512-1520.
  • 5Miele L,Valenza V,La Torre G,Montalto M,Cammarota G,Ricci R,Mascianà R,Forgione A,Gabrieli ML,Perotti G, Vecchio FM,Rapaccini G,Gasbarrini G,Day CP,Grieco A. Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease.Hepatology 2009; 49: 1877-1887.
  • 6Valenti L,Fracanzani AL,Fargion S.The immunopathogenesis of alcoholic and nonalcoholic steatohepatitis:two triggers for one disease? Semin Immunopathol 2009; 31:359-369.
  • 7Brun P,Castagliuolo I,Di Leo V,Buda A,Pinzani M,Palù G,Martines D.Increased intestinal permeability in obese mice:new evidence in the pathogenesis of nonalcoholic steatohepatitis.Am J Physiol Gastrointest Liver Physiol 2007; 292: G518-G525.
  • 8Cani PD,Amar J,Iglesias MA,Poggi M,Knauf C,Bastelica D, Neyrinck AM,Fava F,Tuohy KM,Chabo C,Waget A,Delmée E,Cousin B,Sulpice T,Chamontin B,Ferrières J,Tanti JF,Gibson GR,Casteilla L,Delzenne NM,Alessi MC,Burcelin R.Metabolic endotoxemia initiates obesity and insulin resistance.Diabetes 2007; 56:1761-1772.
  • 9Cani PD,Bibiloni R,Knauf C,Waget A,Neyrinck AM,Delzenne NM,Burcelin R.Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice.Diabetes 2008; 57: 1470-1481.
  • 10Cani PD,Possemiers S,Van de Wiele T,Guiot Y,Everard A, Rottier O,Geurts L,Naslain D,Neyrinck A,Lambert DM, Muccioli GG,Delzenne NM.Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability. Gut 2009; 58:1091-1103.

共引文献18

同被引文献178

引证文献15

二级引证文献81

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部