Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (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
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 Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Leiter, E. H.
Right arrow Articles by Lee, C.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Leiter, E. H.
Right arrow Articles by Lee, C.-H.
Social Bookmarking
 Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes 54:S151-S158, 2005
© 2005 by the American Diabetes Association, Inc.


Section IV: Polygenic Disease and Environment

Mouse Models and the Genetics of Diabetes

Is There Evidence for Genetic Overlap Between Type 1 and Type 2 Diabetes?

Edward H. Leiter1, and Chul-Ho Lee2

1 The Jackson Laboratory, Bar Harbor, Maine
2 Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea

In humans, both type 1 and type 2 diabetes exemplify genetically heterogeneous complex diseases in which epigenetic factors contribute to underlying genetic susceptibility. Extended human pedigrees often show inheritance of both diabetes types. A common pathophysiological denominator in both disease forms is pancreatic ß-cell exposure to proinflammatory cytokines. Hence, it is intuitive that systemically expressed genes regulating ß-cell ability to withstand chronic diabetogenic stress may represent a component of shared susceptibility to both major disease forms. In this review, the authors assemble evidence from genetic experiments using animal models developing clearly distinct diabetes syndromes to inquire whether some degree of overlap in genes contributing susceptibility can be demonstrated. The conclusion is that although overlap exists in the pathophysiological insults leading to ß-cell destruction in the currently studied rodent models, the genetic bases seem quite distinct.


Address correspondence and reprint requests to Dr. Edward H. Leiter, The Jackson Laboratory, 600 Main St., Bar Harbor, ME 04609. E-mail: ehl{at}jax.org

Abbreviations: IL, interleukin; LADA, latent autoimmune diabetes in adults; MHC, major histocompatibility complex; ROS, reactive oxygen species; TNF, tumor necrosis factor


Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2005 by the American Diabetes Association.