Laybutt
Diabetes occurs as a result of pancreatic beta cell failure. In both Type 1 and Type 2 diabetes, beta cell failure is characterised by insulin secretory defects, loss of insulin content and beta cell destruction. In Type 1 diabetes, this is mediated by cytokines that are produced as a part of an autoimmune and inflammatory process. In Type 2 diabetes, elevated lipid and glucose levels occurring as a result of high fat diets, obesity and insulin resistance are thought to contribute. The beta cell is a highly specialised cell with a unique metabolic profile and differentiation specifically geared towards making these cells able to sense fluctuations in circulating glucose levels and secrete insulin accordingly.
Our studies have shown that beta cell secretory defects in diabetes and in islet transplants are associated with a loss of the specialised expression pattern of genes that optimises insulin secretion. However, the molecular and cellular mechanisms responsible for this loss of beta cell differentiation are not known. It has recently emerged that cytokines, lipids and high glucose induce stress within the endoplasmic reticulum (ER) compartment of the cell. Pancreatic beta cells possess a highly developed ER, which is required for the processing, folding and export of vast quantities of newly synthesised insulin. We are investigating ER stress as an exciting potential mechanism for beta cell dysfunction and destruction in both types of diabetes.
Staff
 Research
OfficerDr Caroline Achard |
 PhD StudentMia Akerfeldt |
 PhD StudentJeng Yie (Jenny) Chan |
See also:
Schmitz-Peiffer
Research Group
