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.
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
Mia Åkerfeldt |
Caroline Achard |
| Research Assistant Jeng Yie Chan |
See also:
Schmitz-Peiffer
Research Group
News
Potential to prevent loss of insulin in Type 2 diabetes
MEDIA RELEASE:
14 Jul 2008
Until now, it was thought that the processes leading to the death of insulin-secreting pancreatic cells were similar in both types of diabetes. Scientists at Garvan have now shown that the process is quite different in the two diseases. They have also identified a promising therapeutic target for people with Type 2 diabetes
