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Liver Lipotoxicity And NASH: Mechanistic Roles Of Free Cholesterol, Saturated FFA, JNK1 And TLR4
Funder
National Health and Medical Research Council
Funding Amount
$429,712.00
Summary
Non-alcoholic fatty liver disease (NAFLD) occurs in overweight people, diabetes and with high blood pressure and raised cholesterol. This research is about how cholesterol in liver cells interacts with long chain fatty acids to cause injury and inflammation (steatohepatitis, NASH) in NAFLD.
How Does Dietary Cholesterol Induce Non-alcoholic Steatohepatitis?
Funder
National Health and Medical Research Council
Funding Amount
$802,600.00
Summary
Non-alcoholic fatty liver disease is the most common liver disease that can progress to non-alcoholic steatohepatitis (NASH), cirrhosis and liver cancer. Dietary cholesterol is a major risk factor for NASH. We can demonstrate that cholesterol changes the gut bacteria. These bacteria generate toxic chemicals (bile acids) that signal to the liver and induce NASH. In this project, we use novel ways to clarify the mechanisms of liver inflammation and test novel therapeutic approaches to reverse it.
Inflammatory Pathways To Liver Fibrosis In Non-alcoholic And Alcoholic Steatohepatitis: Reversal By NLRP3 Inhibitors
Funder
National Health and Medical Research Council
Funding Amount
$572,857.00
Summary
Nonalcoholic steatohepatitis (NASH) caused by obesity and diabetes made worse by alcohol, leads to cirrhosis. There is no effective treatment. In mice with NASH, MCC950, a novel drug that blocks NLRP3 (molecule that incites inflammation) reverses liver inflammation and possibly scarring. This proposal will test what activates NLRP3 in NASH, and whether blocking it completely with MCC950 or a new lasting longer inhibitor will dissolve severe liver scarring, and scarring made worse by alcohol.
The Role Of MBOAT7 In Hepatic Inflammation: Implications For Therapy
Funder
National Health and Medical Research Council
Funding Amount
$848,340.00
Summary
When a fatty liver progresses to develop inflammation, patients are at-risk of liver-related morbidity and death. Currently, there are no effective therapies. From human studies, we have discovered that a lipid modifying enzyme (MBOAT7) profoundly regulates liver inflammation. In this proposal, we will obtain a detailed understanding of how the activity of this pathway modulates inflammation. We expect to show that MBOAT7 is a novel ‘druggable’ pathway for the treatment of liver inflammation.
Adipose Distribution, Hepatic Lipid Partitioning And Pathogenesis Of Non-alcoholic Steatohepatitis
Funder
National Health and Medical Research Council
Funding Amount
$133,601.00
Summary
The rising prevalence of obesity and diabetes has led to increase incidence of fatty liver disease and non-alcoholic steatohepatitis (NASH), a form of liver damage that can result in cirrhosis and liver cancer. Currently, approximately 30% people store fat poorly, resulting in increased waist circumference and higher risk of diabetes, cardiovascular disease and NASH. Animal studies are now underway to determine the switch which turns “good fat” to “bad fat”, to identify ways of preventing diabet ....The rising prevalence of obesity and diabetes has led to increase incidence of fatty liver disease and non-alcoholic steatohepatitis (NASH), a form of liver damage that can result in cirrhosis and liver cancer. Currently, approximately 30% people store fat poorly, resulting in increased waist circumference and higher risk of diabetes, cardiovascular disease and NASH. Animal studies are now underway to determine the switch which turns “good fat” to “bad fat”, to identify ways of preventing diabetes, NASH and other adverse outcomes of obesity.Read moreRead less
Manganese is an essential trace element for normal health. However in some medical conditions manganese can build up in the brain and cause a Parkinson's like disease called manganism. Experimental evidence suggests that the liver plays an important role in the development of manganism and this project aims to explore the way the liver handles manganese in health and disease. These studies may assist in understanding how manganism develops.
MECHANISTIC ROLE OF CHOLESTEROL IN NON-ALCOHOLIC STEATOHEPATITIS
Funder
National Health and Medical Research Council
Funding Amount
$533,541.00
Summary
Fatty liver is present in 15-30% of Australians, related to obesity, diabetes and heart attack. Two-thirds of cases reverse easily. The remainder evolve to non-alcoholic steatohepatitis (NASH), liver damage that can lead to cirrhosis and liver failure. This research seeks to find out why some cases of fatty liver lead to NASH, and whether cholesterol that accumulates in the livers of mice with NASH is what causes that damage. If so, we will find new ways to treat NASH by diet or drugs.
Microparticles In NASH: Origins, Pathogenic Roles, And Biomarker Of Disease Activity
Funder
National Health and Medical Research Council
Funding Amount
$540,633.00
Summary
30% of Australians have non-alcoholic fatty liver disease (NAFLD). Cirrhosis is the third cause of death; only 10-25% of NAFLD livers show steatohepatitis (NASH), which leads to cirrhosis. We have found that microparticles (MPs), small fragments of cell membranes, circulate in NASH but not in ordinary fatty liver. We will now explore ways in which MPs incite inflammation and liver fibrosis in NASH, and design new tests based on MPs to improve clinical assessment of patients with NAFLD/NASH.
DPP4 Family Proteases As Drivers Of Chronic Liver Injury
Funder
National Health and Medical Research Council
Funding Amount
$730,041.00
Summary
Type 2 diabetes afflicts over 220 million people and often causes a chronic liver injury. That and hepatitis viruses can cause cirrhosis, liver failure and liver cancer, which is the 2nd most common cause of cancer death. Many Australians suffer from diabetes, fatty liver and/or hepatitis virus infection. We will understand these diseases far better and likely discover a new therapy by assessing roles of the DPP4 family of enzymes in diabetes, fibrosis and fatty liver.