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PMID: 18202132 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Review

Mitochondrial energetics and insulin resistance.

Endocrinology ·Vol. 149 ·No. 3 ·2008-03-00 ·Pages 950-4

Civitarese AE, Ravussin E

Abstract

Obesity, insulin resistance, type 2 diabetes mellitus, and aging are associated with impaired skeletal muscle oxidation capacity, reduced mitochondrial content, and lower rates of oxidative phosphorylation. Several studies have reported ultrastructural abnormalities in mitochondrial morphology and reductions in mitochondrial mass in insulin-resistant individuals. From lower organisms to rodents, mitochondrial membrane structure, function, and programmed cell death are regulated in part by the balance between the opposing forces of mitochondrial fusion and fission, suggesting they may also play an important role in human physiology.

MeSH Terms
Animals Energy Metabolism/physiology Homeostasis/physiology Humans Insulin Resistance/physiology Metalloproteases/physiology Mitochondria, Muscle/physiology Mitochondrial Proteins/physiology
Chemicals
Mitochondrial Proteins Metalloproteases PARL protein, human
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Civitarese Anthony E
Skeletal Muscle Metabolism Laboratory, Human Physiology, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, Louisiana 70808, USA. CivitaAE@pbrc.edu
Ravussin Eric
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Article Info
Journal
Endocrinology
Abbr.
Endocrinology
ISSN
0013-7227
DOI
10.1210/en.2007-1444
Email
civitaae@pbrc.edu
Published
2008-03-00
Epub
2008-00-17
Pages
950-4
Language
English
Region
United States
NLM ID
0375040
PMCID
PMC2275359
Subset
IM
Grants
NIDDK NIH HHS · P30 DK072476 · United States
NIA NIH HHS · U01 AG020478 · United States
NIA NIH HHS · R01 AG20478 · United States
External Links
PubMed source DOI: 10.1210/en.2007-1444 PMC Full Text View journal details
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