Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
529626
Reference Type
Journal Article
Title
Is mitochondrial dysfunction a cause of insulin resistance?
Author(s)
Turner, N; Heilbronn, LK
Year
2008
Is Peer Reviewed?
1
Journal
Trends in Endocrinology and Metabolism
ISSN:
1043-2760
EISSN:
1879-3061
Volume
19
Issue
9
Page Numbers
324-330
Language
English
DOI
10.1016/j.tem.2008.08.001
Abstract
Insulin resistance is a key defect associated with obesity and type-2 diabetes. The precise factors that lead to insulin resistance have not been elucidated fully, but there is a strong association between insulin resistance and inappropriate lipid accumulation in insulin-target tissues. Over the past decade, several studies have reported changes in markers of mitochondrial metabolism in insulin-resistant individuals. These observations have led to the theory that compromised mitochondrial oxidative function, particularly in skeletal muscle, causes excess lipid deposition and the development of insulin resistance. Here, we review the latest findings regarding the link between mitochondrial metabolism and insulin action and, in particular, highlight several recent studies that call into question the cause-and-effect relationship between mitochondrial dysfunction and insulin resistance.
Keywords
human skeletal-muscle; fatty-acid oxidation; intramyocellular; lipid-content; type-2 diabetes-mellitus; stimulated atp synthesis; weight-loss; gamma coactivator-1; calorie restriction; glucose-homeostasis; energy-expenditure
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity