PPARs and the Development of Type 1 Diabetes

被引：23

作者：

Holm, Laurits J. ^{[1
]}

Monsted, Mia Ogaard ^{[1
]}

Haupt-Jorgensen, Martin ^{[1
]}

Buschard, Karsten ^{[1
]}

机构：

[1] Copenhagen Univ Hosp, Dept Pathol, Bartholin Inst, Copenhagen, Denmark

来源：

PPAR RESEARCH | 2020年 / 2020卷

关键词：

PROLIFERATOR-ACTIVATED-RECEPTOR; STIMULATED INSULIN-SECRETION; ENDOPLASMIC-RETICULUM STRESS; ISOLATED PANCREATIC-ISLETS; BETA-CELL FUNCTION; GENE-EXPRESSION; IN-VITRO; T-CELLS; ALTERNATIVE ACTIVATION; TROGLITAZONE PREVENTS;

D O I：

10.1155/2020/6198628

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：

Peroxisome proliferator-activated receptors (PPARs) are a family of transcription factors with a key role in glucose and lipid metabolism. PPARs are expressed in many cell types including pancreatic beta cells and immune cells, where they regulate insulin secretion and T cell differentiation, respectively. Moreover, various PPAR agonists prevent diabetes in the non-obese diabetic (NOD) mouse model of type 1 diabetes. PPARs are thus of interest in type 1 diabetes (T1D) as they represent a novel approach targeting both the pancreas and the immune system. In this review, we examine the role of PPARs in immune responses and beta cell biology and their potential as targets for treatment of T1D.

引用

页数：11

共 165 条

[1] Increased insulin demand promotes while pioglitazone prevents pancreatic beta cell apoptosis in Wfs1 knockout mice [J].