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OBESITY,

INFLAMMATION

AND

INSULIN RESISTANCE

 

IN MEMORIAM OF

MARGARITA LORENZO

 

November 11th, 2010

 

 

 

Registration

on-line

(September 1st to

 October 15th)

Acces


  Updated August 2010             by maria 
 
 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 
Insulin Resistance Research Group
Faculty of Pharmacy
Dept. Biochemistry & Molecular Biology II
 Our Location in Madrid  |  How to contact us  |  Other groups of the department                                           Visit UCM Main-page
 

Introduction


GROUP NAME: OBESITY, INFLAMATION AND INSULIN RESISTANCE

Adipose cells Insulin resistance (a smaller than normal response to a given amount of insulin) is an important contributor to the pathogenesis of type 2 diabetes (T2D), and Obesity a risk factor for developing this disease. The obese state is characterized by what has been called low-grade systemic inflammation. Adipose tissue produces and releases a variety of proinflamatory and anti-inflamatory factors, including the adipokines leptin, adiponectin, resistin and visfating, as well as cytokines and chemokines, such as TNF-alpha, IL-6, IL-1 beta, CRP.

Muscle cells Direct exposure of peripheral tissues to these cytokines through activation of stress kinases and proinflammatory factors, inhibits insulin signalling and induces a state of insulin resistance in several systems including muscle cells and adipocytes, by affecting insulin receptor substrate (IRS) proteins. Regulation involves proteasome-mediated degradation, phosphatase-mediated dephosphorylation and a mechanism involving Ser phosphorylation of IRS-1 that converts IRS-1 in an inhibitor of the insulin receptor Tyr kinase activity. Rosiglitazone is an insulin-sensitizing drug from the family of the thiazolidinediones that has recently been introduced as therapeutic agent for the treatment of T2D.

However, the mechanisms by which this compound restored insulin sensitivity  are not completely understood. Moreover, whether other nuclear receptor agonists could improve insulin action remains to be fully explored. The cellular and animal models that we have developed in our group could be excellent tools for investigating the molecular basis of insulin resistance and the therapeutic potential of these compounds.