Chemically chaperoning the actions of insulin. Trends Endocrinol Metab 2007;18(1):1-3
Date
11/23/2006Pubmed ID
17116401DOI
10.1016/j.tem.2006.11.002Scopus ID
2-s2.0-33845664380 (requires institutional sign-in at Scopus site) 8 CitationsAbstract
The role of inflammation as a mediator of insulin resistance in type 2 diabetes and obesity has been a major focus of studies over the past ten years. In mouse models of obesity and type 2 diabetes, the development of insulin resistance correlates with elevated levels of endoplasmic reticulum stress and induction of the unfolded protein response. Activation of N-terminal C-Jun kinase is known to be associated with unfolded protein response activation, and has been shown to participate in the inhibition of insulin action by stimulating serine phosphorylation of the insulin receptor substrate 1, an event that attenuates insulin signaling. 'Chemical chaperones' are small molecules that have been shown to attenuate unfolded protein response activation. The exciting new findings of Ozcan et al. indicate that chemical chaperones improve glucose tolerance and insulin action in a mouse model of type 2 diabetes. These findings offer a potential new target for therapeutic strategies designed to improve insulin action and glucose tolerance in diabetic individuals.
Author List
Hansen PA, Waheed A, Corbett JAAuthor
John A. Corbett PhD Chair, Professor in the Biochemistry department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBiological Transport
Diabetes Mellitus, Type 2
Enzyme Inhibitors
Humans
Hypoglycemic Agents
Insulin
Insulin Resistance
Models, Biological
Obesity
Signal Transduction
