Dr Carsten Schmitz-Peiffer
Senior Research Fellow; Group Leader, Diabetes and Obesity Program, Garvan Institute of Medical Research; Conjoint Senior Lecturer, Faculty of Medicine, The University of New South Wales
Email: c.schmitz-peiffer 'at' garvan.org.au
Research Group: Schmitz-Peiffer
Carsten's initial research showed an association between protein kinase C activation and lipid-induced insulin resistance in skeletal muscle. Subsequently he demonstrated a causative link between intracellular accumulation of the lipid intermediate ceramide and the inhibition of insulin action caused by the saturated fatty acid palmitate. It is thus clear that different fatty acids act through different mechanisms to reduce insulin sensitivity, and recent findings from his group include a role for particular species of phosphatidic acid.
In addition, the study of mice deficient in protein kinase C epsilon has indicated that this enzyme plays multiple and unexpected roles in the control of blood glucose levels, and the understanding of the diverse mechanisms involved is a major focus of his work.
Education
1990 PhD, University of Bristol, UK
1987 BA (Hons), Cambridge University, UK
Awards and Honours
1987 Smith Kline & French/Bristol University CASE Award
1986 Exibitioner, Natural Sciences, Cambridge University
Publications
Schmitz-Peiffer C, Biden TJ. Protein kinase C function in muscle, liver, and beta-cells and its therapeutic implications for Type 2 diabetes. Diabetes. 2008 57:1774-83.
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.
Cazzolli R, Mitchell TW, Burchfield J, Pedersen, DJ, Turner, N, Biden TJ, Schmitz-Peiffer C. (2007) Dilinoleoyl-phosphatidic acid mediates reduced IRS-1 tyrosine phosphorylation in rat skeletal muscle cells and mouse muscle. Diabetologia 50:1732-42
Taylor A, Ye JM and Schmitz-Peiffer C. (2006) Inhibition of glycogen synthesis by increased lipid availability is associated with subcellular redistribution of glycogen synthase. J. Endocrinol. 188: 11-23.
Schmitz-Peiffer C (2005) Targeting protein kinase C epsilon or theta as a therapeutic strategy for insulin resistance. Drug Discov. Today: Therapeutic Strategies 2:105-110, 2005
Burchfield JG, Lennard AJ, Narasimhan S, Hughes WE, Wasinger VC, Corthals GL, Okuda T, Kondoh H, Biden TJ, and Schmitz-Peiffer C. (2004) Akt mediates insulin-stimulated phosphorylation of Ndrg2 - evidence for crosstalk with protein kinase C theta. J. Biol. Chem. 279: 18623-18632
Cazzolli R, Craig DL, Biden TJ and Schmitz-Peiffer C. (2002) Inhibition Of Glycogen Synthesis In C2C12 Skeletal Muscle Cells By Unsaturated Free Fatty Acid Is Independent Of PKCe, PKCq and b-Oxidation Am. J. Physiol. 282: E1204-1213
Cazzolli R, Carpenter L, Biden TJ, Schmitz-Peiffer C. (2001) A Role for Protein Phosphatase 2A, but not atypical Protein Kinase C zeta, in The Inhibition of Protein Kinase B/Akt and Glycogen Synthesis by Palmitate. Diabetes 50: 2210-2218
Schmitz-Peiffer C (2000) Invited Review: Signalling mechanisms in lipid-induced insulin resistance of skeletal muscle. Cell. Signal. 12: 583-594
Schmitz-Peiffer C, Craig DL, Biden TJ (1999) Ceramide generation is sufficient to account for the inhibition of insulin-stimulated PKB pathway in C2C12 cells pretreated with palmitate. J. Biol. Chem. 274: 24202-24210
Schmitz-Peiffer C, Browne CL, Oakes ND, Watkinson A, Chisholm DJ, Kraegen EW, Biden TJ (1997) Alterations in the expression and cellular localization of protein kinase c isozymes epsilon and theta are associated with insulin resistance in skeletal muscle of the high-fat-fed rat. Diabetes 46: 169-178
