Protein tyrosine phosphatases: molecular switches in metabolism and diabetes

被引：67

作者：

Gurzov, Esteban N. ^{[1
,2
]}

Stanley, William J. ^{[1
,2
]}

Brodnicki, Thomas C. ^{[1
]}

Thomas, Helen E. ^{[1
,2
]}

机构：

[1] St Vincents Inst Med Res, Fitzroy, Vic 3065, Australia

[2] Univ Melbourne, St Vincents Hosp, Dept Med, Fitzroy, Vic 3065, Australia

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2015年 / 26卷 / 01期

基金：

英国医学研究理事会;

关键词：

protein tyrosine phosphatases; metabolism; type; 1; diabetes; 2; LIVER-SPECIFIC DELETION; PANCREATIC BETA-CELLS; DIET-INDUCED OBESITY; GLUCOSE-HOMEOSTASIS; INSULIN-RESISTANCE; LEPTIN RESISTANCE; CANDIDATE GENE; BODY-WEIGHT; SIGNAL TRANSDUCER; ENERGY-BALANCE;

D O I：

10.1016/j.tem.2014.10.004

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Protein tyrosine phosphatases (PTPs) are a large family of enzymes that generally oppose the actions of protein tyrosine kinases (PTKs). Genetic polymorphisms for particular PTPs are associated with altered risk of both type 1 diabetes (T1D) and type 2 diabetes (T2D). Moreover, recent evidence suggests that PTPs play crucial roles in metabolism. They can act as regulators of liver homeostasis, food intake, or immune-mediated pancreatic beta cell death. In this review we describe the mechanisms by which different members of the non-receptor PTP (PTPN) family influence metabolic physiology. This 'metabolic job' of PTPs is discussed in depth and the role of these proteins in different cell types compared. Understanding the pathways regulated by PTPs will provide novel therapeutic strategies for the treatment of diabetes.

引用

页码：30 / 39

页数：10

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