Faculty Advisor

Adams, David S.

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

Accessibility

Unrestricted

Advisor Department

Biology and Biotechnology

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