The Inflammasome In Host Defence And Autoinflammation
Funder
National Health and Medical Research Council
Funding Amount
$408,388.00
Summary
Inflammation is one of the bodies first responses to infection. The inflammasome is a protein complex that activates pro-inflammatory cytokines as part of this process. We are investigating pathogens that activate a specific inflammasome complex, and also an inflammatory disease it may cause when activated accidentally, in the absence of infection. We are also investigating pathways that keep this inflammation in check, and how pathogens might hijack these anti-inflammatory pathways to promote i ....Inflammation is one of the bodies first responses to infection. The inflammasome is a protein complex that activates pro-inflammatory cytokines as part of this process. We are investigating pathogens that activate a specific inflammasome complex, and also an inflammatory disease it may cause when activated accidentally, in the absence of infection. We are also investigating pathways that keep this inflammation in check, and how pathogens might hijack these anti-inflammatory pathways to promote infection.Read moreRead less
The Role Of Insulin Hypersecretion In Beta Cell Dysfunction In Type 2 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$318,622.00
Summary
The treatment of diabetes involves the use of drugs that stimulate the release of insulin from the pancreas to reduce the high blood sugar levels. However, we believe that while in the short term this is a good strategy, in the long-term it damages the cells that produce insulin leading to a worsening state of diabetes. It is the aim of this application to understand the mechanisms by which the insulin producing cells are damaged when forced to oversecrete insulin.
This research proposal will identify changes in liver-secreted proteins during the development of fatty liver, and in the transition from fatty liver to the more advanced form of liver disease, non-alcoholic steatohepatitis (NASH). Understanding the differences in protein secretion between NASH patients and patients with normal/fatty liver will provide the opportunity to identify disease biomarkers that could be determined from a blood sample. This will provide a major shift in clinical care.
Control Of Musculoskeletal Function And Glucose Metabolism By Androgens In Men
Funder
National Health and Medical Research Council
Funding Amount
$245,031.00
Summary
Male sex hormone or androgen deficiency (AD) is a common, but under-diagnosed condition. AD decreases general well being and contributes to muscle weakness, bone fragility and weight gain. By using cutting edge imaging and molecular technologies, we will help to explain the underlying mechanisms of how AD leads to these negative effects. This should ultimately lead to reduction of adverse outcomes of AD, which include fractures and cardiovascular events.
Mitochondrial Energy Metabolism And Insulin Action
Funder
National Health and Medical Research Council
Funding Amount
$380,558.00
Summary
Obesity and type 2 diabetes are two major health conditions associated with abnormal energy metabolism. In this proposal I will investigate the role of important metabolic proteins in regulating energy expenditure and insulin action in skeletal muscle and adipose tissue, two crucial tissues for whole-body energy metabolism. These studies will provide critical insight into the factors leading to obesity and type 2 diabetes and will assist in identifying possible therapeutic targets.
Mechanisms Of Abnormal Expression Of The IGF2 Gene In Disorders Affectin Foetal Growth
Funder
National Health and Medical Research Council
Funding Amount
$420,872.00
Summary
The IGF2 gene is crucial for foetal growth. Only the copy inherited from the father is active, a phenomenon named parental imprinting. In some children with foetal overgrowth or growth retardation, the deregulation of imprinting of the IGF2 gene during the first days of foetal development will influence subsequent growth and will also have major implications in post-natal and adult life. We will investigate the mechanisms resulting in abnormal imprinting of IGF2 early in development.