The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Correspondence
PreviousPrevious
Volume 350:2419-2421 June 3, 2004 Number 23
NextNext

Impaired Mitochondrial Activity and Insulin-Resistant Offspring of Patients with Type 2 Diabetes

Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

 Sign up for free e-toc
 

This Article
-Full Text
- PDF
-PDA Full Text
-Purchase this article

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited
-E-mail When Letters Appear

More Information
-Related Article
 by Petersen, K. F.
-PubMed Citation
To the Editor: Petersen et al. (Feb. 12 issue)1 provide further evidence that insulin resistance is associated with a reduction in mitochondrial function in muscle2 and an increase in lipid content.3 They propose that mitochondrial dysfunction causes lipid accumulation and insulin resistance, but the relation among these variables is probably more complex. For example, insulin can increase mitochondrial transcript levels, protein synthesis, and ATP production in healthy people but not in people with type 2 diabetes.4,5 Thus, one could argue that insulin signaling is required for maintenance of muscle mitochondria and that insulin resistance results in mitochondrial dysfunction, rather than . . . [Full Text of this Article]


This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.