Kathryn Aston-Mourney

Full Name: Dr Kathryn Aston-Mourney
Position Title: Alfred Deakin Research Fellow
Telephone: +61 3 522 72977
Email: k.astonmourney@deakin.edu.au
Campus: Metabolic Research Unit
Geelong at Waurn Ponds
kathryn aston-mourney

 

Research overview

Type 2 diabetes is one of the major health burdens facing the world today. Diabetes is characterised by failure of the insulin producing cells in the pancreas (ß-cells). ß-cell failure is progressive, with patients requiring additional medications over time and eventually insulin injections. Current diabetes treatments cannot stop or slow the progression of ß-cell failure; therefore it is vital that new treatments be developed. Our project aims to generate a ß-cell gene expression signature and use it to screen for novel drugs that will not only effectively treat diabetes but also prevent ß-cell failure. These new improved drugs will improve quality of life and reduce the burden of type 2 diabetes for over 1 million Australians.

Now recruiting Honours and PhD students, please email expressions of interest to: k.astonmourney@deakin.edu.au.

 

Biography

Dr Aston-Mourney completed her PhD in December 2007 at The University of Melbourne, Australia. During this time she examined the physiological and genetic basis of insulin hypersecretion and dysfunction in type 2 diabetes. She then broadened her interest into islet amyloid formation and degradation in type 2 diabetes during her postdoctoral fellowship with Professor Steven Kahn at the University of Washington, USA. In July 2011 Dr. Aston-Mourney returned to Australia where she is now investigating the gene expression signature of dysfunctional ß-cells and potential new drugs for the treatment of type 2 diabetes with Professor Ken Walder at the Metabolic Research Unit at Deakin University.

 

Dr Kathryn Aston-Mourney's Publications

  1. Aston-Mourney K, Hull R.L., Zraika S., Udayasankar J., Subramanian S. L. and Kahn, S.E. Exendin-4 increases islet amyloid deposition but offsets the resultant beta-cell toxicity in human islet amyloid polypeptide transgenic mouse islets. Diabetologia. 2011; 54:1756-65.

  2. Jurgens CA, Toukatly MN, Fligner CL, Udayasankar J, Subramanian SL, Zraika S, Aston-Mourney K, Carr DB, Westermark P, Westermark GT, Kahn SE, Hull RL.ß-Cell Loss and ß-Cell Apoptosis in Human Type 2 Diabetes Are Related to Islet Amyloid Deposition. Am J Pathol. 2011 Jun;178(6):2632-40.

  3. Zraika S, Aston-Mourney K, Marek P, Hull RL, Green PS, Udayasankar J, Subramanian SL, Raleigh DP, Kahn SE. Neprilysin impedes islet amyloid formation by inhibition of fibril formation rather than peptide degradation. JBC. 2010; 285:18177-83.

  4. Hull RL, Zraika S, Udayasankar J, Aston-Mourney K, Subramanian SL, Kahn SE. Amyloid formation in hIAPP transgenic mouse islets and pancreas and human pancreas is not associated with endoplasmic reticulum stress. Diabetologia. 2009; 52:1102-11.

  5. Zraika S, Hull RL, Udayasankar J, Aston-Mourney K, Subramanian SL, Kisilevsky R, Szarek WA, Kahn SE. Oxidative stress is induced by islet amyloid formation and time-dependently mediates amyloid-induced beta cell apoptosis. Diabetologia. 2009;52:626-35.

  6. Udayasankar J, Kodama K, Hull RL, Zraika S, Aston-Mourney K, Subramanian SL, Tong J, Faulenbach MV, Vidal J, Kahn SE. Amyloid formation results in recurrence of hyperglycaemia following transplantation of human IAPP transgenic mouse islets. Diabetologia. 2009; 52:145-53.

 

 

 


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