Postgraduate Studies Projects

Are you interested in why organs turn into toffee with diabetes?  What about finding a real cure for diabetes and its complications?

Advanced glycation is the biochemical reaction which occurs in our bodies to make proteins (and us) grow old.  Although it is a natural process, food chemists also use this reaction to make our food taste better, perhaps most easily recognised as brewed beer, freshly baked bread crusts and vegemite and other golden delights!

Our laboratory uses a variety of approaches including cell culture, molecular biology, genetically modified mice and human clinical studies. We currently have 11 personnel including 2 post-doctoral scientists and 3 PhD students. We have an extremely accomplished track record where our work is published in the very best journals in medical research and attracts regular research funding from both national and international sources.

PhD Projects 2010

Mitochondrial dysfunction as a therapeutic target for diabetes.

Dysfunction of the small power stations or the "mitochondria", within our cells is an extremely important step towards irreversible kidney and islet damage, which affects up to 40% of persons with diabetes.  As our cellular energy levels are depleted, the cells slow down and eventually die.  We have discovered that damage to other cell compartments by advanced glycation (AGEs) can cause and intiate mitochondrial damage and energy depletion from the outside.  Advanced glycation end products (AGEs) are sticky sugar/protein complexes and are abundant with sugar excesses such as that seen with diabetes.  These AGEs interact with receptors and cause the generation of free oxygen radicals within cells, which directly interrupt energy production by mitochondria.  As current therapies do not address this pathway it is a pertinent new target for therapies in diabetes and its complications

A marriage between lifestyle and genetic factors which affect the development of type 2 diabetes.

It is well known that certain lifestyle choices such as high dietary fat and processed foods contribute to the development of diabetes.  Indeed, bad lifestyle choices have worse effects in some individuals which may be related to susceptibility to diabetes which is present within their genetic make up.

Dietary fat and processed foods are extremely high in a group of sugar modifications known as advanced glycation end products (AGEs).  These molecules make our food taste better in addition to providing food chemists and manufacturers with benefits such as longer storage times and less food spoilage. Excessive dietary intake of AGEs has recently been shown to contribute to the development of type 2 diabetes, especially in the context of a high fat diet.  Once in the blood stream dietary AGEs can cause inflammation and free oxygen radical production by binding to specific receptors, including the receptor for AGEs, RAGE.  Indeed, it is even now predicted that defects in the RAGE gene confer susceptibility to diabetes per se.

Honours Project 2010

Increased dietary AGE intake, directly contributes to elevated levels of circulating AGEs which have been implicated as factors which sustain inflammation in humans. We hypothesise that a reduction in dietary AGE intake will improve insulin sensitivity and first phase insulin secretion in overweight individuals by lowering chronic low-grade activation of the immune system (CLAIS).  This project therefore aims to determine the impact of an ~80% change in dietary AGE intake over a period of two weeks in a randomised blinded cross-over study design on circulating AGEs, insulin sensitivity and insulin secretory function in young, healthy obese individuals and also establish whether chronic activation of the immune system plays an intermediary role in the association between AGE intake, insulin sensitivity and secretion.