On type 1 diabetes mellitus pathogenesis

被引:151
|
作者
Paschou, Stavroula A. [1 ]
Papadopoulou-Marketou, Nektaria [1 ]
Chrousos, George P. [1 ]
Kanaka-Gantenbein, Christina [1 ]
机构
[1] Univ Athens, Aghia Sophia Childrens Hosp, Med Sch, Dept Pediat 1,Div Endocrinol Metab & Diabet, Athens, Greece
来源
ENDOCRINE CONNECTIONS | 2018年 / 7卷 / 01期
关键词
type; 1; diabetes; pathogenesis; genetics; autoimmunity; microbiota; BETA-CELL APOPTOSIS; ZINC TRANSPORTER 8; GENETIC SUSCEPTIBILITY; AUTOIMMUNE-DISEASE; ISLET AUTOIMMUNITY; MOLECULAR MIMICRY; RECENT-ONSET; NOD MICE; INSULIN; RISK;
D O I
10.1530/EC-17-0347
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of beta cells of the endocrine pancreas. Pathogenesis of T1DM is different from that of type 2 diabetes mellitus, where both insulin resistance and reduced secretion of insulin by the beta cells play a synergistic role. We will present genetic, environmental and immunologic factors that destroy beta cells of the endocrine pancreas and lead to insulin deficiency. The process of autoimmune destruction takes place in genetically susceptible individuals under the triggering effect of one or more environmental factors and usually progresses over a period of many months to years, during which period patients are asymptomatic and euglycemic, but positive for relevant autoantibodies. Symptomatic hyperglycemia and frank diabetes occur after a long latency period, which reflects the large percentage of beta cells that need to be destroyed before overt diabetes become evident.
引用
收藏
页码:R38 / R46
页数:9
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