Innate immunity, insulin resistance and type 2 diabetes

被引：129

作者：

Fernandez-Real, J. M. ^{[1
,2
,3
]}

Pickup, J. C. ^{[4
]}

机构：

[1] Inst Invest Biomed Girona IdibGi, Dept Diabet Endocrinol & Nutr, Girona 17007, Spain

[2] Univ Hosp Girona Dr Josep Trueta, Girona, Spain

[3] CIBER Fisiopatol Obesidad & Nutr, Madrid, Spain

[4] Guys Hosp, Kings Coll London, Sch Med, Diabet Res Grp, London SE1 9RT, England

来源：

DIABETOLOGIA | 2012年 / 55卷 / 02期

关键词：

Clinical studies; Cytokines; Glucose tolerance; Insulin resistance; Inflammation; Innate immunity; Insulin sensitivity; Macrophages; Pathophysiology; Type; 2; diabetes; SUBCUTANEOUS ADIPOSE; INFLAMMATION; EXPRESSION; GENETICS; DISEASE;

D O I：

10.1007/s00125-011-2387-y

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

In this edition of 'Then and now' the initial studies by J.C. Pickup and colleagues supporting the hypothesis that type 2 diabetes is caused by activated innate immunity, published in Diabetologia in 1997 (40:1286-1292), are discussed. These initial findings led to research that has uncovered links between insulin resistance, obesity, circulating immune markers, immunogenetic susceptibility, macrophage function and chronic infection. Genetic variations leading to the altered production or function of circulating innate immune proteins, cellular pattern recognition receptors and inflammatory cytokines are linked to obesity, insulin resistance and type 2 diabetes. Components of the innate immune system in the muscle, bone, liver and adipose tissue, as well as macrophages, have been revealed to play a role in systemic insulin action. Evolutionary pressures, such as acute infections at the population level (pandemics) and chronic low exposure to environmental products or infectious agents, may have contributed to increased susceptibility and to the current increase in the prevalence of insulin resistance and type 2 diabetes.

引用

页码：273 / 278

页数：6

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