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Understanding the adverse cardio-metabolic effects of glucocorticoids

Dr Angela Xun Nan Chen, Institution: Flinders University

2019 Health Professional Scholarship

Years funded: 2020-2021


Obesity and cardiovascular disease are key health challenges in the 21 century. Recent statistics from the World Health Organization indicate that Australia has the third-highest prevalence of overweight adults in the English-speaking world. This PhD project directly addresses these themes by evaluating the effect of glucocorticoid hormone on obesity and cardiovascular health, with studies that balance clinical application with investigations of underlying mechanisms.

Glucocorticoids are hormones secreted by the adrenal glands glucocorticoid excess increases cardiovascular risk by inducing obesity, diabetes, high cholesterol and high blood pressure and via direct effects on the heart and blood vessels. However, synthetic glucocorticoids, such as prednisolone, are widely used to treat a range of inflammatory diseases such as arthritis and chronic lung disease. The aim of this project is to determine how different clinical and biological aspects of glucocorticoid activity leads to adverse cardiometabolic effects. Manipulation of glucocorticoid action within cardio-metabolic tissues may offer novel therapies to combat cardiovascular disease and obesity. Comprised of three distinct, but linked studies, the results of this PhD project will allow our group to optimise treatment of glucocorticoid excess, thus improving cardiovascular health outcomes.

Study 1 aims to reduce the cardiovascular risk posed by high blood sugars related to synthetic glucocorticoid use in hospitalised patients. Outcomes will directly improve how insulin (a medication used to treat high blood sugars) requirements are calculated to improve blood sugars and reduce the risk of cardiovascular events such as heart attack and cardiac death.

Studies 2 and 3 will evaluate mechanisms underpinning the relationship between glucocorticoid excess, obesity and adverse cardiovascular outcomes. To characterise these mechanisms, we will evaluate patients with adrenal adenomas (benign tumours) that secrete excess glucocorticoid (Study 2) and specific enzyme pathways (11β-hydroxysteroid dehydrogenase enzymes) that may regulate synthetic glucocorticoid activity (Study 3). Study outcomes will provide further guidance and potential novel therapies to reduce glucocorticoid-mediated cardiovascular risk.

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