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Research Topic : tissue specific knockout
Field of Research : Endocrinology
Status : Closed
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  • Funded Activities (21)
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  • Funded Activity

    How Intra-abdominal Transplantation Of Subcutaneous Adipose Tissue Prevents High-fat Diet-induced Insulin Resistance And Obesity

    Funder
    National Health and Medical Research Council
    Funding Amount
    $358,465.00
    Summary
    In obese humans, storing excess fat within the abdomen is associated with the development of adult-onset diabetes and cardiovascular disease. However, the mechanisms linking intra-abdominal fat accumulation with these diseases are not well understood. We have studied intra-abdominal fat accumulation in mice using a transplant model, and we have found that transplanting subcutaneous fat intra-abdominally prevents diet-induced obesity and glucose intolerance. We aim to investigate the underlying m .... In obese humans, storing excess fat within the abdomen is associated with the development of adult-onset diabetes and cardiovascular disease. However, the mechanisms linking intra-abdominal fat accumulation with these diseases are not well understood. We have studied intra-abdominal fat accumulation in mice using a transplant model, and we have found that transplanting subcutaneous fat intra-abdominally prevents diet-induced obesity and glucose intolerance. We aim to investigate the underlying mechanisms.
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    Funded Activity

    Adverse Effects Of Therapeutic Steroids

    Funder
    National Health and Medical Research Council
    Funding Amount
    $119,951.00
    Summary
    The effects of therapeutic glucocorticoid doses on carbohydrate and energy metabolism and cardiovascular risk have not been fully clarified. This PhD thesis will be based around two studies aiming to: 1.) Define mechanisms underlying the adverse effects of low dose prednisolone in patients with inflammatory rheumatologic disease and 2.) Improve treatment of prednisolone-induced hyperglycaemia in hospitalized patients.
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    Funded Activity

    Thyroid-sympathoadrenal Regulation Of Human Brown Fat

    Funder
    National Health and Medical Research Council
    Funding Amount
    $447,141.00
    Summary
    This project aims to determine how hormones influence the growth and activity of brown fat in humans. Majority of fat cells in the body are white fat cells, which store fat, and cause obesity when in excess. Brown fat cells function like generators. They burn fat and release energy as heat. Humans with lots of brown fat are lean. What controls brown fat activity is currently unknown in humans. This project investigates how hormones influence brown fat activity and may shed light on the therapeut .... This project aims to determine how hormones influence the growth and activity of brown fat in humans. Majority of fat cells in the body are white fat cells, which store fat, and cause obesity when in excess. Brown fat cells function like generators. They burn fat and release energy as heat. Humans with lots of brown fat are lean. What controls brown fat activity is currently unknown in humans. This project investigates how hormones influence brown fat activity and may shed light on the therapeutic potential of brown fat in obesity treatment.
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    Funded Activity

    Tissue Hormones That Regulate Blood Flow And Blood Pres Sure

    Funder
    National Health and Medical Research Council
    Funding Amount
    $226,140.00
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    Funded Activity

    Corticotropin Release Inhibitory Factor

    Funder
    National Health and Medical Research Council
    Funding Amount
    $176,549.00
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    Funded Activity

    The Physiological Role Of Calcitonin And Its Receptor In Bone Cell Metabolism.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $496,446.00
    Summary
    Throughout adult life, bone tissue is continuously remodelled. The two main processes involved in bone remodelling, are bone formation and bone breakdown. Bone formation is controlled by cells known as osteoblasts and bone breakdown is controlled by cells known as osteoclasts. Under normal circumstances these two processes are tightly coupled. Excessive breakdown of bone, causes these two processes to become unbalanced and results in bone loss. This is the basis of many bone diseases such as ost .... Throughout adult life, bone tissue is continuously remodelled. The two main processes involved in bone remodelling, are bone formation and bone breakdown. Bone formation is controlled by cells known as osteoblasts and bone breakdown is controlled by cells known as osteoclasts. Under normal circumstances these two processes are tightly coupled. Excessive breakdown of bone, causes these two processes to become unbalanced and results in bone loss. This is the basis of many bone diseases such as osteoporosis, a condition in which the bones become fragile and therefore more susceptible to fracture. 1 in 2 women and 1 in 3 men aged 70 years and older suffer from osteoporosis in Australia. Despite this, the mechanisms which control osteoclast breakdown of bone are not well understood. Our laboratory is interested in how hormones affect osteoclast action. We plan to examine the role of the hormone calcitonin, an important inhibitor of osteoclastic bone breakdown. This will be achieved by studying transgenic mice in which the receptor, or target, for calcitonin is specifically removed from osteoclasts. This will allow us to precisely determine the role of calcitonin in osteoclast function. Data generated by our research group indicates that calcitonin is also involved in controlling bone formation, however, the way in which calcitonin acts on osteoblasts remains poorly understood. Therefore, studying our transgenic mice will also help clarify the role calcitonin plays in bone formation. Current treatment for osteoporosis involves the administration of drugs which inhibit bone breakdown. This project will increase our understanding of how calcitonin acts to regulate bone breakdown and bone formation and may assist in the design of new therapies for osteoporosis. We believe that this research is of great importance as osteoporosis is becoming more prevalent as the population ages.
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    Funded Activity

    Control Of The Production Of Growth Hormone And Related Hormones

    Funder
    National Health and Medical Research Council
    Funding Amount
    $129,683.00
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    Funded Activity

    The Role Of Grb10 In The Regulation Of Muscle Metabolism

    Funder
    National Health and Medical Research Council
    Funding Amount
    $624,960.00
    Summary
    Obesity increases the risk of metabolic diseases such as type 2 diabetes. Muscle is a key tissue for balancing whether energy is used or stored as fat and as we age, muscle mass normally decreases making maintaining a healthy metabolism even more difficult. We have discovered that removing the Grb10 gene from mice produces bigger muscles. This project will investigate the mechanisms of this effect so that strategies can be developed to regulate muscle mass and improve metabolic health
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    Funded Activity

    Kallikrein-like Enzymes In The Uterus

    Funder
    National Health and Medical Research Council
    Funding Amount
    $65,824.00
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    Funded Activity

    Androgen Receptor Signalling In Development And Progression Of Prostate Cancer

    Funder
    National Health and Medical Research Council
    Funding Amount
    $753,420.00
    Summary
    Prostate cancer is a major health problem in Australia, being the second leading cause of cancer deaths in men. Although there have been improvements in the diagnosis and treatment of prostate cancer, there are no effective treatments for advanced (metastatic) disease that has spread to other parts of the body. Currently, the only therapy for advanced disease involves the reduction in circulating androgens such as testosterone by surgical or medical castration, i.e. androgen ablation. Because pr .... Prostate cancer is a major health problem in Australia, being the second leading cause of cancer deaths in men. Although there have been improvements in the diagnosis and treatment of prostate cancer, there are no effective treatments for advanced (metastatic) disease that has spread to other parts of the body. Currently, the only therapy for advanced disease involves the reduction in circulating androgens such as testosterone by surgical or medical castration, i.e. androgen ablation. Because prostate cells are dependent on testicular androgens for their growth and survival, surgical or medical castration results in an initial tumour regression. However, tumours inevitably develop resistance to androgen ablation therapy and regrow. In this study we aim to provide the most comprehensive analysis to date of the role of androgen signalling in the initiation and progression of prostate cancer. This will enable us to identify the most effective means of eliminating androgen-dependent prostate tumours and identify tumours with high metastatic potential. Our studies will indicate whether treatments targeting androgen signalling are a more effective strategy to inhibit prostate cancer growth while minimising undesirable side effects.
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