Faculty Advisor
Adams, David S.
Sponsor
UMass Medical Center
Abstract
Type 1 and Type 2 diabetic patients experience prolonged hyperglycemia punctuated by short episodes of hypoglycemia. These patients develop diabetic complications, which involves loss of normal tissue function. Cell death via the endoplasmic reticulum (ER) stress pathway in response to nutrient availability is a potential mechanism underlying these complications. To understand glucose's role in ER stress in vivo, we induced hypo- and hyper-glycemia in zebrafish embryos, and analyzed normal development and CHOP/GADD153 expression, a major component of ER stress signaling.
Publisher
Worcester Polytechnic Institute
Date Accepted
April 2010
Major
Biology and Biotechnology
Project Type
Major Qualifying Project
Copyright Statement
All authors have granted to WPI a nonexclusive royalty-free license to distribute copies of the work, subject to other agreements. Copyright is held by the author or authors, with all rights reserved, unless otherwise noted.
Accessibility
Unrestricted
Advisor Department
Biology and Biotechnology