The development of insulin resistance in Type 2 diabetes : insights from knockout studies
Pattaranit, Ratchada, Berg, Hugo van den and Spanswick, David. (2008) The development of insulin resistance in Type 2 diabetes : insights from knockout studies. Science Progress, Vol.91 (No.3). pp. 285-316. ISSN 0036-8504Full text not available from this repository.
Official URL: http://dx.doi.org/10.3184/003685008X361343
Diabetes is a common endocrine disorder, primarily characterised by elevated plasma glucose levels. The disease affects all age groups worldwide. Most patients suffer from Type 2 diabetes, which is mainly due to insulin resistance. It is thought that changes in insulin signalling pathways underlie the development of insulin resistance. This article aims to review recent studies that have elucidated the role of individual proteins in these insulin signalling pathways. These studies have been undertaken using two strategies, one employing mice carrying a global null mutation of particular gene-encoding proteins by the homologous recombination method and another strategy using mice with tissue-specific insulin receptor and/or GLUT4 knockout by the Cre-loxP system. The various phenotypes of these knockout mice, and the light they shed on the etiology of insulin resistance, are discussed. By advancing our understanding of the complex molecular mechanisms underlying insulin resistance, these knock-out models may help us to develop more effective treatments for Type 2 diabetes.
|Item Type:||Journal Article|
|Subjects:||Q Science > QA Mathematics|
|Divisions:||Faculty of Science > Mathematics
Faculty of Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016)
Faculty of Science > Centre for Systems Biology
Faculty of Medicine > Warwick Medical School
|Journal or Publication Title:||Science Progress|
|Publisher:||Science Reviews 2000 Ltd.|
|Official Date:||September 2008|
|Page Range:||pp. 285-316|
|Access rights to Published version:||Restricted or Subscription Access|
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