Alterations of Mitochondrial Function and Insulin Sensitivity in Human Obesity and Diabetes Mellitus

Mitochondrial function refers to a broad spectrum of features such as resting mitochondrial activity, (sub)maximal oxidative phosphorylation capacity (OXPHOS), and mitochondrial dynamics, turnover, and plasticity. The interaction between mitochondria and insulin sensitivity is bidirectional and vari...

Full description

Saved in:
Bibliographic Details
Published in:Annual review of nutrition Vol. 36; p. 337
Main Authors: Koliaki, Chrysi, Roden, Michael
Format: Journal Article
Language:English
Published: United States 17.07.2016
Subjects:
Animals
Diabetes Mellitus, Type 1 - metabolism
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - physiopathology
Evidence-Based Medicine
Humans
Insulin Resistance
Mitochondria - enzymology
Mitochondria - metabolism
Mitochondria, Liver - enzymology
Mitochondria, Liver - metabolism
Mitochondrial Turnover
Models, Biological
Non-alcoholic Fatty Liver Disease - etiology
Obesity - metabolism
Obesity - physiopathology
Organ Specificity
Oxidative Phosphorylation
Oxidative Stress
mitochondrial function
bioenergetic adaptation
insulin resistance
oxidative phosphorylation
mitochondrial dynamics
tissue-specificity
ISSN:1545-4312, 1545-4312
Online Access:Get more information
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Mitochondrial function refers to a broad spectrum of features such as resting mitochondrial activity, (sub)maximal oxidative phosphorylation capacity (OXPHOS), and mitochondrial dynamics, turnover, and plasticity. The interaction between mitochondria and insulin sensitivity is bidirectional and varies depending on tissue, experimental model, methodological approach, and features of mitochondrial function tested. In human skeletal muscle, mitochondrial abnormalities may be inherited (e.g., lower mitochondrial content) or acquired (e.g., impaired OXPHOS capacity and plasticity). Abnormalities ultimately lead to lower mitochondrial functionality due to or resulting in insulin resistance and type 2 diabetes mellitus. Similar mechanisms can also operate in adipose tissue and heart muscle. In contrast, mitochondrial oxidative capacity is transiently upregulated in the liver of obese insulin-resistant humans with or without fatty liver, giving rise to oxidative stress and declines in advanced fatty liver disease. These data suggest a highly tissue-specific interaction between insulin sensitivity and oxidative metabolism during the course of metabolic diseases in humans.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1545-4312
1545-4312
DOI:10.1146/annurev-nutr-071715-050656