Abstract
It is generally accepted that mitochondrial dysfunction and endoplasmic reticulum (ER) stress are related to insulin resistance and type 2 diabetes. Mitochondria use substrates from lipid and glucose metabolism in order to generate ATP, and when mitochondrial O2 consumption is decreased due to an altered metabolism there is an increase in reactive oxygen species (ROS) that can impair different types of molecules and cells, especially in β- cells during type 2 diabetes. Furthermore, the maintenance of ER function in insulin-secreting β-cells is crucial, and when ER homeostasis is disrupted, the ER develops an unfolded protein response (UPR) in order to maintain the homeostasis of this organelle. However, when homeostasis fails in mitochondria and ER, these organelles can initiate death signalling pathways. New research has suggested that hyperlipidemia and hyperliglucaemia, known as key factors of type 2 diabetes (T2D), disrupt mitochondrial activity and ER homeostasis, thus triggering a disruption of energy metabolism, unresolvable UPR activation and β-cell death. This review explains the mechanisms of mitochondrial function and ER stress related to the pathological effects of type 2 diabetes in different tissues.
Keywords: Type 2 diabetes, mitochondria, reticulum stress, mitochondria, oxidative stress.
Current Pharmaceutical Design
Title:Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Diabetes
Volume: 22 Issue: 18
Author(s): Milagros Rocha, Noelia Diaz-Morales, Susana Rovira-Llopis, Irene Escribano-Lopez, Celia Bañuls, Antonio Hernandez-Mijares, Evanthia Diamanti-Kandarakis and Victor M. Victor
Affiliation:
Keywords: Type 2 diabetes, mitochondria, reticulum stress, mitochondria, oxidative stress.
Abstract: It is generally accepted that mitochondrial dysfunction and endoplasmic reticulum (ER) stress are related to insulin resistance and type 2 diabetes. Mitochondria use substrates from lipid and glucose metabolism in order to generate ATP, and when mitochondrial O2 consumption is decreased due to an altered metabolism there is an increase in reactive oxygen species (ROS) that can impair different types of molecules and cells, especially in β- cells during type 2 diabetes. Furthermore, the maintenance of ER function in insulin-secreting β-cells is crucial, and when ER homeostasis is disrupted, the ER develops an unfolded protein response (UPR) in order to maintain the homeostasis of this organelle. However, when homeostasis fails in mitochondria and ER, these organelles can initiate death signalling pathways. New research has suggested that hyperlipidemia and hyperliglucaemia, known as key factors of type 2 diabetes (T2D), disrupt mitochondrial activity and ER homeostasis, thus triggering a disruption of energy metabolism, unresolvable UPR activation and β-cell death. This review explains the mechanisms of mitochondrial function and ER stress related to the pathological effects of type 2 diabetes in different tissues.
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Rocha Milagros, Diaz-Morales Noelia, Rovira-Llopis Susana, Escribano-Lopez Irene, Bañuls Celia, Hernandez-Mijares Antonio, Diamanti-Kandarakis Evanthia and M. Victor Victor, Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Diabetes, Current Pharmaceutical Design 2016; 22 (18) . https://dx.doi.org/10.2174/1381612822666160209152033
DOI https://dx.doi.org/10.2174/1381612822666160209152033 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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