Islet inflammation in type 2 diabetes and physiology

被引：279

作者：

Eguchi, Kosei ^{[1
,2
]}

Nagai, Ryozo ^{[3
]}

机构：

[1] Harvard TH Chan Sch Publ Hlth, Dept Genet & Complex Dis, 677 Huntington Ave, Boston, MA 02115 USA

[2] Harvard TH Chan Sch Publ Hlth, Sabri Ulker Ctr, 677 Huntington Ave, Boston, MA 02115 USA

[3] Jichi Med Univ, Shimotsuke, Tochigi, Japan

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2017年 / 127卷 / 01期

关键词：

TOLL-LIKE RECEPTOR; OBESITY-INDUCED INFLAMMATION; BETA-CELL PROLIFERATION; GROWTH FACTOR-A; NLRP3; INFLAMMASOME; FATTY-ACID; TISSUE INFLAMMATION; INSULIN-RESISTANCE; METABOLIC SYNDROME; TRANSGENIC MICE;

D O I：

10.1172/JCI88877

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The finding of islet inflammation in type 2 diabetes (T2D) and its involvement in beta cell dysfunction has further highlighted the significance of inflammation in metabolic diseases. The number of intra-islet macrophages is increased in T2D, and these cells are the main source of proinflammatory cytokines within islets. Multiple human studies of T2D have shown that targeting islet inflammation has the potential to be an effective therapeutic strategy. In this Review we provide an overview of the cellular and molecular mechanisms by which islet inflammation develops and causes beta cell dysfunction. We also emphasize the regulation and roles of macrophage polarity shift within islets in the context of T2D pathology and beta cell health, which may have broad translational implications for therapeutics aimed at improving islet function.

引用

页码：14 / 23

页数：10

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