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Dysregulated ghrelin signalling in pancreatic β-cells under hyperuricemic conditions – the cause for the onset of type 2 diabetes mellitus?

A postgraduate research opportunity at the University of Otago.

Details

Close date
Friday, 8 December 2017
Academic background
Health Sciences
Host campus
Dunedin
On-campus or via distance?
On-campus
Qualification
PhD
Department
Physiology
Supervisor
Dr Andrew Bahn

Overview

Ghrelin is mainly secreted by the stomach and by binding to the growth hormone receptor it controls growth hormone release, feeding and adiposity. Interestingly, ghrelin is also secreted from pancreatic β-cells, and it controls in an autocrine fashion glucose induced insulin secretion (GIIS).

We have previously established that elevated plasma levels of uric acid (hyperuricemia), a metabolic end-product known to cause gout, contribute to impaired insulin secretion via increase of AMP-kinase (AMPK) expression and phosphorylation. Moreover, hyperuricemia leads to pancreatic β-cell death mediated by AMPK and an elevated miR-34a expression.

We are now interested in identifying the molecular link between hyperuricemia, insulin secretion and β-cell survival mediated by uric acid transporter GLUT9 to further decipher mechanisms responsible for the onset of type 2 diabetes.

Several projects are available which will involve hyperuricemic and/or hyperglycaemic mouse models and cell model studies combining different animal, molecular biological, cell culture and hormone assay techniques. Students who are interested in the topic and keen to meet a challenge to perform state of the art research on causes for the onset of type 2 diabetes mellitus are encouraged to apply.

Contact

Dr Andrew Bahn
Email   andrew.bahn@otago.ac.nz