Abstract
Introduction: Obesity and type 2 diabetes are growing health problems worldwide. The three principal diabetogenic factors are adiposity, insulin resistance in skeletal muscle, and decreased insulin production by pancreatic β cells. During recent years, macroautophagy (hereafter autophagy) — sequestration and lysosomal degradation of cellular components — has emerged as an important player in these processes, playing a protective role against development of insulin resistance and diabetes. Of particular importance is the removal of dysfunctional mitochondria via mitophagy, a form of macroautophagy selective for mitochondria. Both muscle insulin resistance and β-cell dysfunction largely depend on metabolic overload of mitochondria, which results in incomplete β-oxidation, oxidative stress, accumulation of toxic lipid intermediates, and mitochondrial damage. Mitophagy eliminates this vicious cycle of oxidative stress and mitochondrial damage, and thus counteracts pathogenic processes. Autophagy also mediates exercise-induced increases in muscle glucose uptake and protects β cells against ER stress in diabetogenic conditions. On the other hand, adipose tissue autophagy promotes adipocyte differentiation, possibly through its role in mitochondrial clearance. Being involved in many aspects, autophagy appears to be an attractive target for therapeutic interventions against obesity and diabetes.
Conclusion: Here we explore the connections of autophagy with mitochondria in obesity and type 2 diabetes, and discuss its roles in diabetic complications. Understanding how autophagy protects against diabetes could help design new strategies against this growing epidemic.Keywords: Macroautophagy, mitophagy, diabetes, muscle, adipose tissue, beta cells.
Current Diabetes Reviews
Title:Autophagy and Mitochondria in Obesity and Type 2 Diabetes
Volume: 13 Issue: 4
Author(s): Jaakko Sarparanta, Marina García-Macia and Rajat Singh*
Affiliation:
- Department of Medicine (Endocrinology), and Molecular Pharmacology, Member of the Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Forchheimer Building, Room 505D, Bronx, NY 10461,United States
Keywords: Macroautophagy, mitophagy, diabetes, muscle, adipose tissue, beta cells.
Abstract: Introduction: Obesity and type 2 diabetes are growing health problems worldwide. The three principal diabetogenic factors are adiposity, insulin resistance in skeletal muscle, and decreased insulin production by pancreatic β cells. During recent years, macroautophagy (hereafter autophagy) — sequestration and lysosomal degradation of cellular components — has emerged as an important player in these processes, playing a protective role against development of insulin resistance and diabetes. Of particular importance is the removal of dysfunctional mitochondria via mitophagy, a form of macroautophagy selective for mitochondria. Both muscle insulin resistance and β-cell dysfunction largely depend on metabolic overload of mitochondria, which results in incomplete β-oxidation, oxidative stress, accumulation of toxic lipid intermediates, and mitochondrial damage. Mitophagy eliminates this vicious cycle of oxidative stress and mitochondrial damage, and thus counteracts pathogenic processes. Autophagy also mediates exercise-induced increases in muscle glucose uptake and protects β cells against ER stress in diabetogenic conditions. On the other hand, adipose tissue autophagy promotes adipocyte differentiation, possibly through its role in mitochondrial clearance. Being involved in many aspects, autophagy appears to be an attractive target for therapeutic interventions against obesity and diabetes.
Conclusion: Here we explore the connections of autophagy with mitochondria in obesity and type 2 diabetes, and discuss its roles in diabetic complications. Understanding how autophagy protects against diabetes could help design new strategies against this growing epidemic.Export Options
About this article
Cite this article as:
Sarparanta Jaakko, García-Macia Marina and Singh Rajat*, Autophagy and Mitochondria in Obesity and Type 2 Diabetes, Current Diabetes Reviews 2017; 13 (4) . https://dx.doi.org/10.2174/1573399812666160217122530
DOI https://dx.doi.org/10.2174/1573399812666160217122530 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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