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Professor Trevor Biden

 

Principal Research Fellow; Director, Diabetes Signalling Unit; Group Leader, Cell Signalling Group, Diabetes and Obesity Research Program, Garvan Institute of Medical Research; Associate Professor, Faculty of Medicine, The University of New South Wales

Email: t.biden 'at' garvan.org.au
Research Group: Biden

 
 
Trevor Biden undertook his PhD on insulin secretion in London, following relocation of his mentor’s laboratory from Sydney University. Subsequently, as a post-doc with Claes Wollheim in Geneva, he was introduced to signal transduction, and contributed to early studies characterising IP3 as a second messenger. Shifting both fields and location, Biden returned to Australia and set up a lab at the Garvan where he successfully cloned PKCiota, the last of the PKC family to be discovered.
 
 
 

In ensuing years, Trevor's original group has developed into a Unit, but still continues to focus on the nexus between signalling, cellular function and the pathophysiology of diabetes, be it investigating the molecular mechanisms of insulin resistance, or pancreatic beta cell dysfunction. He believes that the team’s current projects - endoplasmic reticulum stress in beta cells, and the surprising re-emergence of PKC as a therapeutic target for diabetes, are some of the most exciting of his career.

Education

1983 PhD University of London, London, UK
1979 BSc (Hons) University of Sydney

Awards and Honours

1989-92 Juvenile Diabetes Foundation International Career Development Award
1987-89 Queen Elizabeth II Australian National Research Fellowship

Publications

Cantley, J., Burchfield, J.G., Pearson, G.L. Schmitz-Peiffer, C., Leitges, M., and Biden, T.J. Deletion of PKCe selectively enhances the amplifying pathways of glucose-stimulated insulin secretion via increased lipolysis in mouse _-cells. Diabetes 2009; 58, 1826-34

Preston, A.M., Gurisik, E., Bartley, C., Laybutt, D.R. and Biden, T.J. Reduced ER-to-Golgi protein trafficking contributes to ER stress in lipotoxic beta cells by promoting protein overload. Diabetologia 2009; 52, 2369-73

Schmitz-Peiffer C, Laybutt DR, Narasimhan S, Burchfield JG, Mitchell CJ, Gurisik E, Braun U, Cooney GJ, Leitges M and Biden TJ. Inhibition of PKCe improves glucose-stimulated insulin secretion and reduces insulin clearance. Cell Metab. 2007 6, 320-328.

Laybutt, DR, Preston AM, Akerfeldt MC, Busch AK, Biankin AV, and Biden, T.J. Endoplasmic Reticulum Stress Contributes to ≤-Cell Apoptosis in Type 2 Diabetes. Diabetologia 2007; 50, 752-763

Busch AK, Gurisik E, Cordery DV, Sudlow M, Denyer GS, Laybutt DR, Hughes WE, Biden TJ. Increased fatty acid desaturation and enhanced expression of stearoyl coenzyme A desaturase protects pancreatic beta-cells from lipoapoptosis. Diabetes 2005; 54(10):2917-24.

Busch AK, Cordery D, Denyer GS, Biden TJ. Expression-profiling of palmitate- and oleate-regulated genes provides novel insights into the effects of chronic lipid exposure on pancreatic β-cell function. Diabetes 2002; 51:977-987.

Carpenter L, Cordery D, Biden TJ. Protein kinase C δ activation by interleukin-1β stabilizes inducible nitric-oxide synthase mRNA in pancreatic β-cells. J Biol Chem 2001; 276:5368-5374.

Schmitz-Peiffer C, Craig DL, Biden TJ. Ceramide generation is sufficient to account for the inhibition of insulin-stimulated PKB pathway in C2C12 skeletal muscle cells pretreated with palmitate. J Biol Chem 1999; 274:24202-24210.

Schmitz-Peiffer C, Browne CL, Watkinson A, Oakes ND, Chisholm DJ, Kraegen EW, Biden TJ. Alterations in the expression and cellular localization of protein kinase C isozymes θ and ε are associated with insulin resistance in skeletal muscle of the high-fat-fed rat. Diabetes 1997; 46:169-178.

Selbie LA, Schmitz-Peiffer C, Sheng Y, Biden TJ. Molecular cloning and characterization of PKCi, an atypical isoform of protein kinase C derived from insulin-secreting cells. J Biol Chem 1993; 268:24296-24302.

 

Search for all publications by Trevor Biden

 
 
 

Areas of Interest

signalling, protein kinases, protein kinase C, protein phosphorylation, insulin secretion, pancreatic beta cells, islets of Langerhans, lipotoxicity, endoplasmic reticulum stress, apoptosis, Type 2 diabetes, Type 1 diabetes
 

News

 

Potential to prevent loss of insulin in Type 2 diabetes

MEDIA RELEASE: 14 Jul 2008
Until now, it was thought that the processes leading to the death of insulin-secreting pancreatic cells were similar in both types of diabetes. Scientists at Garvan have now shown that the process is quite different in the two diseases. They have also identified a promising therapeutic target for people with Type 2 diabetes
 
 

Solving a critical part of the insulin puzzle

MEDIA RELEASE: 04 Oct 2007
We are now one step closer to improved treatment of Type 2 diabetes following significant findings made by scientists at the Garvan Institute of Medical Research. The team from Garvan's Diabetes Signalling Unit, led by Associate Professor Trevor Biden and Dr Carsten Schmitz-Peiffer, has identified a very important biological target that will enable them to address one of the major underlying causes of diabetes.
 
 

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