Endoplasmic reticulum stress and type 2 diabetes.

Abstract:

:Given the functional importance of the endoplasmic reticulum (ER), an organelle that performs folding, modification, and trafficking of secretory and membrane proteins to the Golgi compartment, the maintenance of ER homeostasis in insulin-secreting β-cells is very important. When ER homeostasis is disrupted, the ER generates adaptive signaling pathways, called the unfolded protein response (UPR), to maintain homeostasis of this organelle. However, if homeostasis fails to be restored, the ER initiates death signaling pathways. New observations suggest that both chronic hyperglycemia and hyperlipidemia, known as important causative factors of type 2 diabetes (T2D), disrupt ER homeostasis to induce unresolvable UPR activation and β-cell death. This review examines how the UPR pathways, induced by high glucose and free fatty acids (FFAs), interact to disrupt ER function and cause β-cell dysfunction and death.

journal_name

Annu Rev Biochem

authors

Back SH,Kaufman RJ

doi

10.1146/annurev-biochem-072909-095555

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

767-93

eissn

0066-4154

issn

1545-4509

journal_volume

81

pub_type

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