Laybutt
Interestingly, the majority of overweight individuals do not develop
type 2 diabetes because their pancreatic beta cells compensate
with enhanced insulin secretion. It is the failure of beta cells
compensation that is fundamental to the development of diabetes. 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.
We propose that in susceptible individuals, a gradual rise in blood
glucose (hyperglycaemia) and lipid levels resulting from increasing
obesity and insulin resistance leads to a loss of the unique gene
expression pattern that is necessary for appropriate insulin secretion.
This exacerbates hyperglycaemia, which causes beta cell
dedifferentiation and eventually the death of beta cells by apoptosis.
Our group has recently found evidence in several models of diabetes
that supports this hypothesis. We have identified and are investigating
novel candidate genes that potentially link hyperglycaemia to the
development of impaired beta cell function. Furthermore, we are
investigating endoplasmic reticulum (ER) stress as an exciting
potential mechanism for beta cell destruction in type 1 and type 2
diabetes.
Staff
Mia Åkerfeldt |
Visiting Student Jennifer Howes |
See also:
Schmitz-Peiffer
Research Group
