Beta Cell Stress Group

The failure of pancreatic beta cells causes type 2 diabetes, as well as type 1 diabetes. Our research is focussed on determining how an adaptive response to stress helps beta cells increase insulin release and protect against diabetes. Our research is significant because it will advocate the targeting of specific components of the cell stress response as a novel approach to restore and protect functional beta cells for diabetes therapy.

Research project available (PhD, Masters, Honours)

  • Type 2 diabetes is a metabolic disease caused by the failure of pancreatic beta cells to produce insulin, resulting in chronically elevated blood glucose levels. Being overweight or obese is a risk factor for type 2 diabetes. However, only a relatively small fraction of overweight/obese individuals develops type 2 diabetes. Normally, beta cells compensate for increased insulin demand by an adaptation in beta cell mass and insulin secretion. Diabetes arises only in subjects that fail to sustain the compensatory response. However, the mechanisms that govern beta cell compensation and failure are poorly defined. This project will aim to determine the mechanisms of beta cell compensation and failure during the progression to type 2 diabetes in order to discover novel strategies to protect against the disease.
  • Beta cells contain highly developed endoplasmic reticulum due to heavy engagement in insulin biosynthesis and secretion. In response to stress within the endoplasmic reticulum, the unfolded protein response is activated. This project will examine the role of endoplasmic reticulum stress and the unfolded protein response in beta cell function and survival. XBP1 is a key mediator of the unfolded protein response. We will examine the role of XBP1 in the determination of beta cell identity.

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