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leaD researcher
Burks, Deborah
Fundación Centro de Investigación Príncipe Felipe
C/ Eduardo Primo Yúfera, 3 46013 Valencia
(+34) 96 328 96 80 [email protected] group Website
gROUP MEMBERS
Staff members: Acosta Umanzor, Carlos Rene | Arámbul Anthony, María José | Noon, Luke
Associated members: González Navarro, Herminia | Leal Tassias, Aránzazu | Moreno Gimeno, Inmaculada
Main lines of research
Our research focuses on insulin receptor substrate (IRS) proteins which are the major intracellular targets of the activated insulin receptor. Loss of Irs2 in both mice and humans is associated with a reduced mass of pancreatic beta cells and peripheral insulin resistance, hallmarks of diabetes.
Our core research consists of 4 major lines:
1) Regulation of beta cell compensation and pancreas regeneration. Given that proliferation of existing beta cells represents the fundamental mechanism for beta cell compensation, it is important to precisely define the signals which govern cell-cycle machinery in the endocrine pancreas. Recently, we have observed that IRS2 signals are essential for the regulation of the cyclin kinase CDK4 in beta cells.
2) The role of IRS2 signals in obesity-induced inflammation. Female Irs2-deficient mice display a dysregulation of appetite due to the role of IRS2 signals in the hypothalamus and thus, develop moderate obesity. We are currently characterizing the inflammation components that are regulated directly by the insulin resistance resulting from loss of Irs2. Also, Irs2-deficient mice have more adipose progenitors but these fail to differentiate to mature adipocytes.
3) Hepatic insulin resistance, liver regeneration, and mechanisms of nAFLD. Throughout the lifetime of an individual, adult stem cells represent a mechanism for the maintenance and regeneration of tissues. One of our objectives is to identify the molecular mechanisms by which insulin signaling modulates proliferation and differentiation of progenitor cells in insulin-sensitive tissues. These results may provide tools for maintaining stem cell function in the presence of aging-related and pathologic changes in metabolism.
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