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Trends Endocrinol Metab. 2015 Aug;26(8):438-48. doi: 10.1016/j.tem.2015.05.007. Epub 2015 Jun 12.

Targeting endoplasmic reticulum stress in insulin resistance.

Author information

1
Department of Pharmacology and Therapeutic Chemistry, Faculty of Pharmacy, University of Barcelona, Institute of Biomedicine of the University of Barcelona (IBUB), Barcelona, Spain; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain.
2
Department of Pharmacology and Therapeutic Chemistry, Faculty of Pharmacy, University of Barcelona, Institute of Biomedicine of the University of Barcelona (IBUB), Barcelona, Spain; Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain. Electronic address: mvazquezcarrera@ub.edu.

Abstract

The endoplasmic reticulum (ER) is involved in the development of insulin resistance and progression to type 2 diabetes mellitus (T2DM). Disruption of ER homeostasis leads to ER stress, which activates the unfolded protein response (UPR). This response is linked to different processes involved in the development of insulin resistance (IR) and T2DM, including inflammation, lipid accumulation, insulin biosynthesis, and β-cell apoptosis. Understanding the mechanisms by which disruption of ER homeostasis leads to IR and its progression to T2DM may offer new pharmacological targets for the treatment and prevention of these diseases. Here, we examine ER stress, the UPR, and downstream pathways in insulin sensitive tissues, and in IR, and offer insights towards therapeutic strategies.

KEYWORDS:

apoptosis; endoplasmic reticulum stress; inflammation; insulin resistance; type 2 diabetes mellitus; unfolded protein response

PMID:
26078196
DOI:
10.1016/j.tem.2015.05.007
[Indexed for MEDLINE]

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