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Sphingosine Kinase As A Target Therapeutic For Obesity Induced Insulin Resistance
Funder
National Health and Medical Research Council
Funding Amount
$450,390.00
Summary
Obesity is linked to the development of insulin resistance and diabetes, which represent a significant health issue in Australia. A number of factors contribute to the development of insulin resistance, including defective fatty acid metabolism. This study proposes to investigate whether manipulating sphingosine kinase, a key enzyme in lipid metabolism, affects the development of insulin resistance. These studies may identify novel targets for the treatment of insulin resistance and diabetes.
Circulating Ceramides, Inflammation And Insulin Resistance
Funder
National Health and Medical Research Council
Funding Amount
$358,319.00
Summary
Ceramides are a type of fat that are stored in the body. When people store too many ceramides in their muscles and liver they no longer respond normally to insulin, which leads to the development of type 2 diabetes. Ceramide levels are increased in the blood of people with type 2 diabetes. The aim of the this project is to determine whether ceramides in the blood contribute to type 2 diabetes and whether reducing ceramide levels in the blood improves health.
Adipose Triglyceride Lipase: Regulation And Implications For The Aetiology Of Insulin Resistance
Funder
National Health and Medical Research Council
Funding Amount
$323,453.00
Summary
Obese individuals have elevated fat levels in the blood and muscle, which contributes to the development of other diseases such as type 2 diabetes. A newly discovered protein named adipose triglyceride lipase (ATGL) is essential for fat breakdown. This project aims to identify how ATGL operates and determine whether defective ATGL function leads to type 2 diabetes. These studies will assist in the development of strategies aimed at reducing fatty acids in blood and muscle.
Identifying A Novel Role For Pigment Epithelium-derived Factor In Obesity-related Metabolic Dysfunction
Funder
National Health and Medical Research Council
Funding Amount
$361,637.00
Summary
Obesity is an important factor contributing to insulin resistance and type 2 diabetes; however, the factors linking these disorders are not well defined. A protein called PEDF is elevated in obesity and type 2 diabetes. This project will examine how PEDF causes insulin resistance and whether blocking PEDF's actions prevents insulin resistance. Successful completion of this project may lead to therapeutics that reduce the risk of developing type 2 diabetes.
Function And Pathophysiological Role Of A Novel Glucose Transporter Expressed In Skeletal Muscle
Funder
National Health and Medical Research Council
Funding Amount
$216,412.00
Summary
Diabetes is a disorder of metabolism resulting from a combination of deficiency of insulin and defective action of the insulin that is present. The most prominent metabolic abnormality is high blood glucose, which is often not satisfactorily corrected by insulin treatment. One of the main reasons for the high blood glucose is reduced uptake of glucose by muscle tissue. The mechanism by which insulin enhances glucose entry into muscle cells involves mobilisation of a specific protein from the glu ....Diabetes is a disorder of metabolism resulting from a combination of deficiency of insulin and defective action of the insulin that is present. The most prominent metabolic abnormality is high blood glucose, which is often not satisfactorily corrected by insulin treatment. One of the main reasons for the high blood glucose is reduced uptake of glucose by muscle tissue. The mechanism by which insulin enhances glucose entry into muscle cells involves mobilisation of a specific protein from the glucose transporter protein family, which has been designated GLUT4. Surprisingly, animals that have been genetically altered to eliminate orknockout GLUT4 production do not develop diabetes. This finding has led to the theory that there is a backup glucose transporter protein that can prevent diabetes when there is a problem with GLUT4 function. We have recently discovered a new member of the glucose transporter protein family that could potentially function as either a parallel or a backup system for GLUT4. This new glucose transporter, which we have called GLUT8, is present in human muscle tissue and studies in other cells have shown that it alters its distribution within the cell in reponse to insulin. We now want to study in more detail the role of this new glucose transporter in muscle tissue and how it functions compared with GLUT4. In particular, we think it is possible that Type 2 diabetes occurs when there is not only a problem with the mobilisation of GLUT4 but also a defect in the production or function of GLUT8. If this is the case, then increasing GLUT8 production might improve glucose transport into muscle tissue and so improve control of blood glucose levels in diabetes.Read moreRead less
Osteocytes, the most abundant and long-lived, yet least studied bone cell, are increasingly recognised as key controllers of bone remodelling and are implicated in many bone diseases. Our work is uncovering novel molecular and cellular pathways by which osteocytes act and survive in bone, which is generally an oxygen-deprived tissue. This will provide a rational basis to seek improved treatments of bone disease.