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The Role Of Urotensin II In Diabetes-Associated Atherosclerosis
Funder
National Health and Medical Research Council
Funding Amount
$405,594.00
Summary
People with diabetes most commonly die from stroke or heart attack and we need to determine what makes them more prone to these problems. The recently discovered UII system is increased in people with diabetes and has been found in diseased parts of blood vessels. Thus, the aim of this project is to characterise the UII system in the setting of diabetes using 2 unique genetically altered mice and a blocker a to study the effects of high cholesterol, diabetes and a deletion of UII.
Type 2 diabetes is caused by multiple genetic defects, resulting in high blood sugar levels. These high sugar levels are primarily due to a decrease in the concentration of insulin, a hormone produced by the pancreas. A number of recent studies have aimed to identify which genes are regulated under conditions that mimic diabetes. One gene shown to have altered expression levels under these conditions is an enzyme called fructose-1,6-bisphosphatase (or FBPase). This enzyme is involved in the meta ....Type 2 diabetes is caused by multiple genetic defects, resulting in high blood sugar levels. These high sugar levels are primarily due to a decrease in the concentration of insulin, a hormone produced by the pancreas. A number of recent studies have aimed to identify which genes are regulated under conditions that mimic diabetes. One gene shown to have altered expression levels under these conditions is an enzyme called fructose-1,6-bisphosphatase (or FBPase). This enzyme is involved in the metabolism of sugar and is usually expressed at undetectable levels in the pancreas, but when blood sugar levels are high, the amount of FBPase in the pancreas increases considerably. We hypothesise that this increase in FBPase may contribute to the decrease in insulin secretion by the pancreas, seen in the diabetic state. The aim of this proposal therefore is to study mice that we have modified to express increased FBPase specifically in the pancreas, in order to determine whether this will lead to a decrease in insulin release and to diabetes. If this is the case, then FBPase could be targeted for the development of drugs that would improve the control of blood sugar levels in diabetes.Read moreRead less
Exploring Models For Antibody Mediated Endocrine Disease
Funder
National Health and Medical Research Council
Funding Amount
$140,949.00
Summary
Common endocrine disorders like Graves’ disease, are mediated by auto-antibodies, causing uncontrolled hormonal expression and undesirable effects. However, due to the limited understanding of the antibody interactions, the treatment is still focused on controlling the hormone production/interactions instead of targeting the underlying autoimmune processes. This project aims to further characterise the role the antibody through animal studies and developing novel treatments based on the research ....Common endocrine disorders like Graves’ disease, are mediated by auto-antibodies, causing uncontrolled hormonal expression and undesirable effects. However, due to the limited understanding of the antibody interactions, the treatment is still focused on controlling the hormone production/interactions instead of targeting the underlying autoimmune processes. This project aims to further characterise the role the antibody through animal studies and developing novel treatments based on the research.Read moreRead less
Identification And Characterisation Of A Gene Causing Insulin Hypersecretion In A Mouse Model Of Diabetes Susceptibility
Funder
National Health and Medical Research Council
Funding Amount
$430,320.00
Summary
Diabetes is a disorder primarily characterised by the inability to produce and secrete the pancreatic hormone insulin, which regulates plasma sugar levels. This results in increased sugar levels which cause diabetic complications such as retinopathy and nephropathy. The inability to produce and secrete insulin is due to both defects in function as well as a reduction in pancreatic beta cells. Paradoxically it has been shown that some patients who are at risk of develping diabetes actually secret ....Diabetes is a disorder primarily characterised by the inability to produce and secrete the pancreatic hormone insulin, which regulates plasma sugar levels. This results in increased sugar levels which cause diabetic complications such as retinopathy and nephropathy. The inability to produce and secrete insulin is due to both defects in function as well as a reduction in pancreatic beta cells. Paradoxically it has been shown that some patients who are at risk of develping diabetes actually secrete more insulin than normal. Furthermore it has been suggested that this increase in insulin secretion actually may be associated with the decreased production and secretion of insulin characteristic of diabetes. The DBA-2 mouse is a model of reduced insulin production and secretion when exposed to high sugar levels or diabetes. However we have shown that in the normal non-stressed state DBA-2 mice actually secrete more insulin than normal and that this occurs from a very early age, suggesting that this trait is inherited. We have subsequently performed genetic studies and have identified a segment of DNA containing 10 genes associated with increased insulin secretion in DBA-2 mice. The level of one of these genes we have called Hip1 is increased 5-fold in DBA-2 mice, providing a candidate gene for increased insulin secretion in this model of diabetes susceptibility. However, whether Hip1 is also responsible for reduced insulin production and secretion in the DBA-2 mouse is not known. Therefore the overall hypothesis of this project is that the gene Hip1 which is associated with increased insulin secretion is also responsible for reduced insulin production and secretion when DBA-2 mice are exposed to high sugar or obesity. Determining why Hip1 is increased and whether it results in diabetes in DBA-2 mice may provide a reasonable candidate for the development of therapeutic interventions which may prevent the progression of diabetes in some patients.Read moreRead less
Targeting TGF-beta proteins to control animal reproduction. This project aims to develop a suite of novel biologics to control fertility in female mammals. This project expects to demonstrate that targeting a single class of ovarian proteins will enhance or inhibit egg production. The expected outcomes of this project are to (1) transform the breeding of livestock animals, which should provide significant benefits to the agricultural industry, through increased herd/flock sizes, and (2) provide ....Targeting TGF-beta proteins to control animal reproduction. This project aims to develop a suite of novel biologics to control fertility in female mammals. This project expects to demonstrate that targeting a single class of ovarian proteins will enhance or inhibit egg production. The expected outcomes of this project are to (1) transform the breeding of livestock animals, which should provide significant benefits to the agricultural industry, through increased herd/flock sizes, and (2) provide a non-surgical method of contraception in companion/feral species, which should address the large unmet need for fertility control in these animals.
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Brain Regulation of Reproduction: Challenging the ‘KNDy’ Hypothesis. The brain switches reproduction on and off by changing the frequency of pulses of gonadotrophin releasing hormone. The processes that produce the pulses have been a puzzle for decades but, recently, brain cells that produce three peptides (kisspeptin, neurokinin B, dynorphin), known as ‘KNDy cells’, have been heralded as the ‘missing link’, or even the ‘pulse generator’. Using sheep, this project will challenge the KNDy hypothe ....Brain Regulation of Reproduction: Challenging the ‘KNDy’ Hypothesis. The brain switches reproduction on and off by changing the frequency of pulses of gonadotrophin releasing hormone. The processes that produce the pulses have been a puzzle for decades but, recently, brain cells that produce three peptides (kisspeptin, neurokinin B, dynorphin), known as ‘KNDy cells’, have been heralded as the ‘missing link’, or even the ‘pulse generator’. Using sheep, this project will challenge the KNDy hypothesis with pheromones and with acute increases in nutrition, two factors that rapidly increase the frequency of gonadotrophin releasing hormone pulses. The outcomes of this research are directly relevant to the optimisation of reproductive management in farm animals, wildlife and humans.Read moreRead less
Hypothalamic Signalling In Cortical And Trabecular Bone Anabolic Activity
Funder
National Health and Medical Research Council
Funding Amount
$472,770.00
Summary
Osteoporosis is a disease associated with an exponential rise in the number of fractures in the elderly. These fractures are so common that around 1 in 3 women and 1in four men will be affected. They cause pain, disability that can be permanent disability and are associated with premature death. Current treatments are able to effectively increase bone strength in osteoporotic patients but can not return bone strength to normal. Some new treatments can restore bone strength to some extent but the ....Osteoporosis is a disease associated with an exponential rise in the number of fractures in the elderly. These fractures are so common that around 1 in 3 women and 1in four men will be affected. They cause pain, disability that can be permanent disability and are associated with premature death. Current treatments are able to effectively increase bone strength in osteoporotic patients but can not return bone strength to normal. Some new treatments can restore bone strength to some extent but these are limited by expense and safety concerns. We have discovered a pathway in the brain that reduces bone formation and by blocking this pathway we can achieve doubling of the amount of bone in key bone sites. This occurs due to a marked increase in the amount of new bone formed. In fact, genetic manipulation of this pathway was able to double the speed at which bone is made by the skeleton. Excitingly, these increases in bone were possible in adult mice, suggesting such changes could be potential therapy for human patients. However, in order to be able to harness this pathway we must understand what molecules within the brain are responsible for the signals that reach the bone. Our proposal aims to identify the nerve signalling molecule(s) and the receptor for these signals within the brain that initiates the increase in bone formation. This project ultimately aims to identify a target for new therapies that could cause this beneficial effect by administration of a simple treatment, preferably by mouth in adult humans.Read moreRead less
Type 2 Diabetic Renal Complications And Microvascular Injury: Novel Predictors Of Onset And Progression, Mechanisms Of Association With Cardiovascular Disease And The Benefits Of Fenofibrate.
Funder
National Health and Medical Research Council
Funding Amount
$84,448.00
Summary
We will investigate the mechanisms of diabetic complications related to kidney and blood vessel disease, focusing on identifying people at greater risk and ways to improve or prevent these complications. In addition, we will look at how diabetic kidney disease affects non-kidney related problems like heart disease and examine the benefit of fenofibrate on both. This greater understanding will aid further drug development in kidney and cardiovascular diseases.
Accelerated Telomere Length Attrition Rate In Diabetes And Its Cellular Mechanism
Funder
National Health and Medical Research Council
Funding Amount
$38,381.00
Summary
I am a PhD in Medicine-University of Sydney. My research focus is about telomere dynamic, its mechanism and correlation between telomere length and diabetes attributes. I will compare telomere length between different diabetes groups & examine telomere regulation in cell culture/animal model to compliment my clinical data. The hypothesis: accelerated telomere shortening may co-segregate with diabetes complications and by preserving telomere we could potentially prevent adverse effect of diabetes
This study aims to identify naturally occurring genetic variations between men which modify the impact of testosterone, the major male hormone, on men's health and medical care. This study will examine new factors which determine how much any particular man may gain benefit from testosterone exposure such as in muscle and bone development as well as suffer detrimental effects on cardiovascular and prostate diseases. This may clarify some new aspects of how men's health is determined as well as d ....This study aims to identify naturally occurring genetic variations between men which modify the impact of testosterone, the major male hormone, on men's health and medical care. This study will examine new factors which determine how much any particular man may gain benefit from testosterone exposure such as in muscle and bone development as well as suffer detrimental effects on cardiovascular and prostate diseases. This may clarify some new aspects of how men's health is determined as well as developing new, customized medical treatments for men.Read moreRead less