期刊文献+

肠道菌群与儿童1型糖尿病关系的研究进展 被引量:1

Advances in research on relationship between intestinal flora and childhood type 1 diabetes mellitus
原文传递
导出
摘要 1型糖尿病(type 1 diabetes mellitus,T1DM)是胰岛β细胞被破坏而导致胰岛素绝对缺乏所致。T1DM绝大多数属于自身免疫性疾病,由遗传及环境因素共同参与其发病过程。儿童糖尿病95%以上为T1DM。近年来儿童T1DM发病率呈现逐年上升趋势。研究表明肠道菌群与儿童T1DM的发病密切相关,T1DM儿童肠道菌群分布失调,肠道菌群可能通过影响肠道免疫系统和改变肠壁通透性来参与T1DM的发病过程。动物实验的研究中,改变肠道菌群分布和应用益生菌可以预防和延缓T1DM的发病。干预肠道菌群是否会预防、延缓儿童T1DM的发生尚需要进一步的研究,希望干预肠道菌群能为预防和治疗儿童T1DM提供新的方向。 Type 1 diabetes mellitus(T1 DM) is caused by the absolute deficiency of insulin due to destruction of islet β cells. The vast majority of T1 DMs are an autoimmune disease. Genetic and environmental factors are involved in the pathogenesis of T1 DM. More than 95% of childhood diabetes mellitus is type 1 diabetes. The incidence of T1 DM in children has been increasing year by year. Studies have shown that intestinal flora is closely related to the onset of T1 DM in children. The distribution of intestinal flora in children with T1 DM is disordered, which may participate in the pathogenesis of T1 DM by affecting the intestinal immune system and changing intestinal wall permeability. In animal experiments, changes in the distribution of intestinal flora and use of probiotics can prevent and delay the onset of T1 DM. Whether the intervention of intestinal flora can prevent and delay the occurrence of T1 DM in children needs be further studied. It is expected that the intervention of intestinal flora can provide a new direction for the prevention and treatment of T1 DM in children.
作者 李琳珊 苏芊 霍珊 常波 LI Linshan;SU Qian;HUO Shan;CHANG Bo(Department of Endocrinology,Dalian Children s Hospital,Dalian,Liaoning 116012,China)
出处 《中国微生态学杂志》 CAS CSCD 2019年第12期1475-1478,1482,共5页 Chinese Journal of Microecology
关键词 肠道菌群 1型糖尿病 儿童 肠壁通透性 肠道免疫 Intestinal flora Type 1 diabetes mellitus Children Intestinal wall permeability Intestinal immune
  • 相关文献

参考文献5

二级参考文献73

  • 1Lijin Liang,Evette B,Gerald J.The phosphodiesterase inhibitors pentoxifylline and rolipram prevent diabetes in NOD mice[J].Diabetes,1988,47:570-575
  • 2Sai P,Rivereau AS,Granier C,et al.Immunization of nonobese diabetic(NOD)mice with glutamic acid decarboxylase-derived peptide 524-543 reduces cyclophosphamide accelerated diabetes[J].Clin Exp Immunol,1996,105:330-337
  • 3Wang B,Gonzalez A,Benoist C,et al.The role of CD8^+ T cells in the initiation of insulin-dependent diabetes[J].Eur J Immunol,1996,26:1 762-1 769
  • 4Wong F S,Visintin I,Flavell R A,et al.CD8^+ T cell clones can transfer rapid onset of diabetes in NOD mice in the absence of CD4^+ T cell[J].J Exp Med,1996,183:67-76
  • 5Benoist C,Mathis D.Cell death mediators in autoimmune diabetes shortage of suspects[J].Cell,1997,89:1-3
  • 6Perdigon G,Vintinie,Alarez S,Study of the possible mechanisms involved in the mucosal immune system activation by lactic acid bacteria[J].Journal of Dairy Science,1999,82:1 180-1 114
  • 7Makino S,Kunimoto Y.Breeding of nonobese strain of mice[J].Exp Anim,1980,29:1 213
  • 8Lichtman SM. Bacterial translocation in humans [J]. J Pediatr Gastroenterol Nutr, 2001,33:1-10.
  • 9Farhadi A, Banan A, Fields J, et al. Intestinal barrier: An interface between health and disease [ J]. J Gastroenterol Hepatol, 2003, 18: 479-497.
  • 10Visser J, Rozing J, Sapone A, et al. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms [J]. Ann N Y Acad Sci, 2009, 1165:195-205.

共引文献28

同被引文献5

引证文献1

二级引证文献1

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