Sweet taste is generally associated with calorie rich diet. In the brain this information is used to adjust the amount of food that is eaten and how hungry one feels. Disrupting this balance by supplementing food with artificial sweeteners, which have no caloric content, represents a challenge for the brain. However, specific neuronal pathways are in place to correct this imbalance of calorie to taste and we are interested to identify the major component of these pathways.
The Mechansim Of Cachexia Induced By The TGF-b Superfamily Cytokine, MIC-1
Funder
National Health and Medical Research Council
Funding Amount
$544,200.00
Summary
MIC-1 is a protein first cloned and characterised by our research group. It belongs to the TGF beta protein superfamily which is very important in development of cancer, wound - fracture healing and inflammation. Recent evidence also suggests it can act as an appetite suppressant, and this is especially relevant in conditons like cancer where it is overproduced. This project seeks to understand the mechanisms for its capacity to modify appetite
The project aims to understand how a factor responsible for the production of a type of white blood cell interacts with its receptor. If we knew the molecular details of how this factor works then we would be able to control better diseases, such as osteoporosis and arthritis, where such cells can play havoc by destroying tissue. The project also has implications for certain leukaemias which lose growth control mechanisms in response to this factor.
Last year an estimated 3.1 million people died of AIDS (source: UNAIDS, Dec 2002) equivalent to the number killed by tuberculosis and malaria combined. AIDS-related opportunistic infections (OIs) are the main cause of death for AIDS patients, especially in resource constrained countries where access to antiretroviral and antibiotic therapy is limited. Attempts to limit the epidemic have failed and new foci have emerged in Eastern Europe, Central Asia and, of particular relevance for us, South Ea ....Last year an estimated 3.1 million people died of AIDS (source: UNAIDS, Dec 2002) equivalent to the number killed by tuberculosis and malaria combined. AIDS-related opportunistic infections (OIs) are the main cause of death for AIDS patients, especially in resource constrained countries where access to antiretroviral and antibiotic therapy is limited. Attempts to limit the epidemic have failed and new foci have emerged in Eastern Europe, Central Asia and, of particular relevance for us, South East Asia, underlining the fact that safe and effective treatment for AIDS-related OIs will be a global health priority for the foreseeable future. People with healthy immune systems do not get OIs since the germs that cause such infections are efficiently ingested and subsequently destroyed by cells called macrophages. We have discovered that the virus that causes AIDS, HIV-1, interferes with the ability of macrophages to ingest opportunistic pathogens by the 2 most important mechanisms used for this purpose. We believe that this is the direct cause for the susceptibility of AIDS patients to many of the opportunistic pathogens that cause their OIs. The purpose of this grant will be to understand the biochemical basis underlying these 2 defects in macrophage function. This will help in the design of safe, adjunctive therapies aimed at improving macrophage function and reducing the risk of HIV-infected individuals developing AIDS-related OIs.Read moreRead less