I am a graduate student in BSc Applied Microbiology (2008). I have a background in with metabolic physiology as I published research in Mycopathologia (2009), and I am highly interested in your area of research. Moreover, I have recently acquired a graduate diploma from Monash University Australia (2018), one of the oldest and most prestigious higher learning facilities in the country, with a 70% average grade in reproductive biology. I decided to pursue my PhD position in your institution, following the positions announced in your website.
The project is attractive and promising, so I have immense interest in enrolling on it under your supervision since a close relationship exists between my career interests and the project hypothesis. In my studies, I have made great progress towards a deeper understanding of the molecular basis obesity and diabetes. However, the existing knowledge is grossly inadequate, especially in identifying the key link between type 2-diabetes and obesity. The research interest explores the coupling of the two diseases and in turn creates interest in the adipose tissue, a major contributing factor to the onset of obesity and metabolic diseases like diabetes.
My published research contributes to the growing body of literature in the last 20 years, which posit that caveolae have an important function for release of adiponectin via an exosomal pathway. Enrolling in the PhD program will enable me to contribute further in the discipline by in determining how the adipose tissue, which plays vital roles such as mechanical protection and fuel storage, acts as an endocrine organ through the production of leptin and adiponectin hormones. The former hormone improves the sensitivity of insulin in key target tissues, regulates the metabolism of energy, and modulates inflammatory responses. Interestingly, genetic factors affect a high percentage of adiponectin plasma levels. High levels of the hormone in human plasma correlates to a lower risk of type 2-diabetes. It also lowers the likelihood of insulin resistance and metabolic flexibility, which is essentially the ability to adjust to any changes in the sum of nutrients in the body and switch between lipids and carbohydrates with the increase of the primary fuel source. Lower levels of the hormone leads to metabolic impairment. The hypothesis of the PhD program project is, therefore, interesting as it investigates adiponectin secretion and its relation to understanding the mechanisms affecting metabolism diseases.
Enrollment to the program will provide me with an opportunity to conduct research in highly motivated environments in well equipped laboratories, and under comprehensive mentoring opportunities. Such opportunities would provide me with career development as a researcher in metabolic physiology. It is already established that adiponectin and leptin hormones regulate the body's sensitivity to insulin. My previous research reported that adiponectin and leptin follow different secretory routes as seen from the examination of intercellular trafficking pathways that secret each hormone. Distinct intercellular compartments are responsible for the secretion of each hormone, whereby adiponectin is secreted from the endosomal compartments. Advanced research in the secretion of the two hormones will create a major breakthrough in the treatment of metabolic diseases, and joining your PhD class will provide me with an excellent opportunity to be on the wonderful team that makes the groundbreaking discovery to revolutionalize modern medicine.
For more information highlighting my academic background, I have attached my resume. Thank you for taking the time to read my email and I look forward to your response.
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