Recipient Of 2012 Australian Liver Foundation-Hospitality Industry Career Development Research Fellowship
Dr David Frazer
Iron Metabolism Laboratory
Queensland Institute of Medical Research (QIMR)
Dr David Frazer obtained his undergraduate degree in Applied Science (with Honours) from the Queensland University of Technology in 1997. Following this he began his PhD on the regulation of iron homeostasis at QIMR under the supervision of Professor Greg Anderson.
He was awarded his PhD entitled “The molecular basis of intestinal iron absorption and its regulation” in 2003 and has since continued working in the area of iron in health and disease in the Iron Metabolism Laboratory at QIMR.
During this time, Dr Frazer’s principle research area has been investigating the factors regulating the production of a molecule called hepcidin by the liver.
This molecule is of central importance in maintaining body iron levels as it regulates the amount of iron absorbed from the diet. The importance of hepcidin is evident in pathological conditions such as hereditary haemochromatosis.
This inherited condition affects 1 in 200 Australians of Caucasian descent and is caused by mutations in a gene called HFE. While the precise function of HFE is not known, in 2003 Dr Frazer’s research showed that when HFE is disrupted there is a reduction in hepcidin production by the liver, resulting in an increase in dietary iron absorption.
As a consequence, iron loading occurs in various tissues throughout the body, particularly the liver, and this can result in tissue damage and organ failure if untreated.
Other conditions in which inappropriate hepcidin production contributes to disease include the iron loading anaemias such as ß-thalassaemia.
These patients have reduced red blood cell viability and attempt to compensate for this by increasing red blood cell production, a process that requires large amounts of iron.
The body tries to allow for this by decreasing hepcidin production and increasing iron absorption. However, the extra iron entering the body leads to tissue iron loading.
The mechanism by which developing red blood cells in the bone marrow signal changes in hepcidin expression in the liver is not yet known and is the current focus of Dr Frazer’s research.
During the next three years Dr Frazer will continue to focus on unravelling the molecular mechanism by which changes in red blood cell production alter hepcidin expression in the liver.
This research will not only try to determine the identity of the soluble molecule(s) produced by the developing red blood cells in the bone marrow that signals the cells of the liver to alter hepcidin expression, but will also examine the components within liver cells that are responsible for altering hepcidin expression in response to such signalling molecules.
A greater knowledge of how this pathway regulates hepcidin production by the liver should lead to the development of better treatment options for patients with iron loading disorders.
The Career Development Fellowship awarded by the Australian Liver Foundation through the generous support of the Hospitality Industry in Queensland will allow Dr Frazer to continue his important work for a further three years.
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