Prof Trevor Biden
Principle Research Fellow
Following an undergraduate degree in Biochemistry at the University of Sydney Professor Trevor Biden undertook his PhD with Keith Taylor at London Hospital Medical College. He subsequently worked as a post-doc during a very productive era in Claes Wollheim’s lab in Geneva. Following a short sojourn at the Australian National University in Canberra, Trevor commenced his own independent lab at the Garvan Institute. Over time he has trained many PhDs and post-docs, some of whom now head their own closely aligned labs within the Garvan.
Trevor has a long-standing international reputation in the area of basic beta cell biology. He has made important contributions in the areas of regulating insulin secretion and beta cell apoptosis, and his work straddles both T1D and T2D. In recent years he has been instrumental in elucidating and characterizing the contribution of ER stress to beta cell dysregulation. He is now extending his research focus more broadly in beta cell biology to encompass studies in autophagy and lysosomal biology, as well as inflammation.
He holds several patents and has worked closely with several pharmaceutical/biotech companies. In the last 5 years he has served on the Editorial Advisory Board or as Associate Editor for the two leading journals in diabetes field, Diabetes and Diabetologia. He has made an extensive and ongoing contribution to grant review panels with both JDRFI and NHMRC.
In the NewsGarvan Institute scientists receive $10.7 million in NHMRC funding - Oct 22, 2014
How fat could help solve part of the diabetes problem - Oct 29, 2013
Garvan receives $15.5 million in NHMRC funding round - Oct 25, 2013
Potential to prevent loss of insulin in Type 2 diabetes - Jul 14, 2008
1979 - BSc Hons, University of Sydney - Australia
Pearson, G., Mellet, N., Davenport, A., Cantley, J., Bourbon, P., Cosner, C., Helquist, P., Meikle, P.J., and Biden, T.J. (2014) Lysosomal acid lipase and lipophagy are constitutive negative regulators of glucose-stimulated insulin secretion from pancreatic b-cells. Diabetologia. In press
Boslem, E.,MacIntosh, G., Preston, A.M., Bartley, C., Busch, A.K., Fuller, M., Laybutt. D.R., Meikle, P.J., and Biden, T.J. (2011) A lipidomic screen of palmitate-treated MIN6 b-cells links sphingolipid metabolites with endoplasmic reticulum (ER) stress and impaired protein trafficking. Biochem. J. 435: 267-276.
Preston, A.M., Gurisik, E., Bartley, C., Laybutt, D.R. and Biden, T.J. (2009) Reduced ER-to-Golgi protein trafficking contributes to ER stress in lipotoxic beta cells by promoting protein overload. Diabetologia 52: 2369-73
Laybutt, D.R., Preston, A.M., Åkerfeldt, M.C., Kench, J.G., Busch, A.K., Biankin, A.V., and Biden, T.J. (2007) Endoplasmic Reticulum Stress Contributes to b-Cell Apoptosis in Type 2 Diabetes. Diabetologia 50: 752-763.
Schmitz-Peiffer, C., Laybutt, D.R., Burchfield, J.G., Gurisik, E., Narasimhan, S., Mitchell, C.J., Braun, U., Cooney, G.J., Leitges, M. and Biden, T.J. (2007) Inhibition of PKCε improves glucose-stimulated insulin secretion and reduces insulin clearance. Cell Metab. 6: 320-328.
Busch, A.K., Gurisik, E., Cordery, D.V, Sudlow, M. Denyer, G.S., Hughes, W.E., and Biden, T.J. (2005) Increased fatty acid desaturation and enhanced expression of stearoyl CoA desaturase protects pancreatic b-cells from lipoapoptosis Diabetes 54: 2917-2924.
Busch, A-K., Cordery, D., Denyer, G. and Biden, T.J. (2002) Expression-profiling of palmitate- and oleate-regulated genes following chronic lipid exposure on pancreatic b-cell function. Diabetes 51: 977-987.
Schmitz-Peiffer, C., Craig, D. and Biden, T.J. (1999) Ceramide generation is sufficient to account for the inhibition of the insulin-stimulated PKB pathway in C2C12 skeletal muscle cells pretreated with palmitate. J. Biol. Chem. 274: 24202-24210.
Schmitz-Peiffer, C., Browne, C.L., Oakes, N.D., Watkinson, A., Chisholm, D.J., Kraegen, E.W. and Biden, T.J. (1997) Alterations in the expression and cellular localization of protein kinase C isozymes e and q are associated with insulin resistance in skeletal muscle of the high-fat-fed rat. Diabetes 46, 169-178.
Selbie, L.A., Schmitz-Peiffer, C., Sheng, Y., and Biden, T.J. (1993) Molecular cloning and characterization of PKCi, an atypical isoform of protein kinase C derived from insulin-secreting cells. J. Biol. Chem. 268: 24296-24302.
Biden, T.J., Peter-Riesch, B., Schlegel, W. and Wollheim, C.B. (1987) Ca2+ -mediated generation of inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate in pancreatic islets: studies with K+, glucose and carbamylcholine. J. Biol. Chem. 262, 3567-71.
Wollheim, C.B. and Biden, T.J. (1986) Second messenger function of inositol 1,4,5-trisphosphate: early changes in inositol phosphates, cytosolic Ca2+ and insulin release in carbamylcholine-stimulated RINm5F cells. J. Biol. Chem. 261: 8314-8319.
Biden, T.J. and Wollheim, C.B. (1986) Ca2+ regulates the inositol tris/tetrakisphosphate pathway in intact and broken preparations of insulin-secreting RINm5F cells. J. Biol. Chem. 261: 11931-11934.
Biden, T.J., Prentki, M., Irvine, R.F., Berridge, M.J. and Wollheim, C.B. (1984) Inositol 1,4,5-trisphosphate mobilizes intracellular Ca2+ from permeabilized insulin-secreting cells. Biochem. J. 223: 467-473.
Prentki, M., Biden, T.J., Janjic, D., Irvine, R.F., Berridge, M.J. and Wollheim, C.B. (1984) Rapid mobilization of Ca2+ from rat insulinoma microsomes by inositol 1,4,5-trisphosphate. Nature 309: 562-564.