Metabolic Wiring In Adipocytes - Unique Role In Maintaining Long-term Health
Funder
National Health and Medical Research Council
Funding Amount
$1,077,886.00
Summary
Fat cell metabolism is wired to optimize the cell’s ability to make and store lipid while programming the cell to fulfil its function in whole body metabolism. We will: 1) map fat cell metabolism under optimal and insulin resistant conditions; 2) explore the role of 3 nodes in his metabolic circuit predicted as control points; 3) use a novel genetically engineered mouse model to explore the functional significance of fat cell metabolism in whole body insulin sensitivity.
Most common diseases of ageing like diabetes and cancer have proven intractable because much of our knowledge is limited to individual molecules. This proposal takes a global approach to complex diseases, utilising quantitative high-resolution methods and computational modelling. This research will lead to a completely new way of thinking about complex diseases providing a range of completely novel treatment options.
Transcription-based Identification Of Insulin Resistance Subtypes
Funder
National Health and Medical Research Council
Funding Amount
$341,883.00
Summary
A key feature of type 2 diabetes is the failure of metabolic tissues such as muscle and fat to respond to normal levels of insulin. This 'insulin resistance' is caused by a number of mechanisms. We will use cutting-edge technology to identify small sets of genes that define each variety of insulin resistance. These gene sets will be used to diagnose sub-types of insulin resistance and will facilitate the development of personalised therapies to effectively treat individuals with type 2 diabetes.
Ciliary Neurotrophic Factor: A Novel Theraputic Agent For The Prevention Of Muscle Insulin Resistance
Funder
National Health and Medical Research Council
Funding Amount
$602,673.00
Summary
In 1995 leptin was discovered and scientists world-wide hoped that this was the great panacea in the treatment of obesity related disorders. Alas, from 1995-1997 the identification of a novel cytokine inducible compound termed suppressor of cytokine signaling (SOCS) that negatively regulated leptin signalling and lead to leptin resistance, quashing hopes for a viable anti-obesogenic drug. Recently, however, work from our group has demonstrated that the neuropoietic cytokine, ciliary neurotrophic ....In 1995 leptin was discovered and scientists world-wide hoped that this was the great panacea in the treatment of obesity related disorders. Alas, from 1995-1997 the identification of a novel cytokine inducible compound termed suppressor of cytokine signaling (SOCS) that negatively regulated leptin signalling and lead to leptin resistance, quashing hopes for a viable anti-obesogenic drug. Recently, however, work from our group has demonstrated that the neuropoietic cytokine, ciliary neurotrophic factor (CNTF), can act in an anti-obesogenic fashion in a manner similar to leptin. However, unlike leptin, when we place rodents on a high fat diet, the effects of CNTF persist and override induction SOCS proteins. This project will examine the biochemical pathways that allow the actions of CNTF to persist in the presence of diet-induced obesity. This is of major significance because in completing this work, the potential for the development of peripheral tissue drug targets for the treatment of obesity related diseases are both tangible and realistic.Read moreRead less
I am a cell biologist-whole body physiologist determining the cellular and molecular mechanisms that lead to insulin resistance in insulin sensitive tissues such as skeletal muscle, liver and adipose tissue. My work primarily focuses on the role of inflam
Targeting Skeletal MTORC1 As A Novel Approach For The Treatment Of Diet-induced Insulin Resistance
Funder
National Health and Medical Research Council
Funding Amount
$586,979.00
Summary
Diet-induced insulin resistance is a pathology that underlies type 2 diabetes. Elucidating the pathways and tissues that contribute to this condition is crucial for drug development. The skeleton has emerged as a critical insulin target tissue. We provide evidence that suppression of mTORC1, a complex over-activated by nutrients, in bone cells improves insulin sensitivity. In this study, we will determine if blocking mTORC1 function in bone cells can treat diet-induced insulin resistance.
The Role Of Estrogen-receptor Alpha (ERa) In The Pathogenesis Of Diabetes And Cardiovascular Disease.
Funder
National Health and Medical Research Council
Funding Amount
$374,757.00
Summary
Cardiovascular disease (CVD), including heart attack and stroke, causes more deaths in Australia than any other disease. A major risk factor for CVD is diabetes, which affects more than 1 million Australians. Therefore, treating diabetes will reduce the number of people likely to die from CVD. This project aims to investigate a recently identified role for estrogen in the protection against diabetes. If successful, findings from this project may lead to new treatments against diabetes and CVD.