help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Endocrinology, doi:10.1210/en.2007-1444
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
149/3/950    most recent
Author Manuscript (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Civitarese, A. E.
Right arrow Articles by Ravussin, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Civitarese, A. E.
Right arrow Articles by Ravussin, E.
Endocrinology Vol. 149, No. 3 950-954
Copyright © 2008 by The Endocrine Society


Minireview

Minireview: Mitochondrial Energetics and Insulin Resistance

Anthony E. Civitarese and Eric Ravussin

Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808

Address all correspondence and requests for reprints to: Anthony E. Civitarese, Skeletal Muscle Metabolism Laboratory, Human Physiology, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, Louisiana 70808. E-mail: CivitaAE{at}pbrc.edu.

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.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2008 by The Endocrine Society