IUB Diabetes Research Group seminar – Wed., 2/17 at 2pm

The IUB Diabetes Research Group would like to invite you to a seminar as part of the Indiana University-Bloomington Diabetes Research Group Seminar Series.

All are welcome to attend. Snacks and drinks will be provided.

Event:  Seminar talk by Patrick T. Fueger, PhD ​, Associate Professor of Pediatrics and Cellular & Integrative Physiology and Co-Director, Bioengineering Interdisciplinary Training Program for Diabetes Research

Title:  “Targeting feedback control mechanisms to restore glucose homeostasis in diabetes”

Date:  Wednesday, February 17, 2016

Time:  2:00-3:00 pm

Where:  Social Science Research Commons Grand Hall (Woodburn Hall 200), 1100 E. 7th Street, Bloomington, IN

The mission of the Fueger laboratory is to identify molecular mechanisms regulating glucose homeostasis during health and disease (e.g., diabetes).  To do this, we have research programs aimed at: 1) preventing metabolic dysregulation in insulin responsive tissues such as skeletal muscle and liver, and 2) maintaining and restoring functional beta cell mass.  We have a particular interest in endogenous, negative feedback regulators of pathways (i.e. molecular brakes) and are investigating how these proteins modulate cellular survival, repair, regeneration, and function.  Currently we have been focusing our efforts on the cell cycle inhibitor p21 and the EGFR inhibitor Mig6 (Mitogen-inducible gene 6, or errfi1).  All of our work fits within a framework of using cellular and molecular techniques to explore integrative physiology and metabolism.   We are actively exploring how Mig6: 1) contributes to the demise of functional beta cell mass during glucolipotoxicity associated with type 2 diabetes, 2) compromises beta cell survival, function, and regeneration in type 1 diabetes, and 3) impairs hepatic survival and regeneration during obesity and hyperlipidemia associated with type 2 diabetes.  We are also trying to discover novel beta cell growth factors and mediators of cellular survival and repair.  It is our ultimate goal to establish that targeting endogenous feedback inhibitors can be an efficacious strategy for improving the overall health and function of metabolic tissues.