It is generally accepted that insulin resistance must be considered as the consequence of multiple defects of the insulin signalling cascade. Principally, these defects may occurr at all levels of insulin action starting with the insulin receptor and leading to the downstream effector systems. In this context, insulin-regulated glucose uptake and the translocation of glucose transporters is subject to a very prominent alteration.
Recent findings support the notion that individual segments of the insulin signalling cascade can be modified by pharmacological agents, making it likely that a specific and causal prevention of insulin resistance may be achieved.
To reach this goal, the extended analysis of the insulin signalling cascade, the identification of novel molecular targets, and the assessment of the pathogenesis of insulin resistance are mandatory.

The group runs several research projects related to different aspects of cellular signal transduction, vesicular translocation of glucose transporters and the pathogenesis of insulin resistance. This includes cell and molecular biology studies on normal and aberrant insulin action using heart and skeletal muscle cells, and additional projects concerning the pharmacological modulation of the insulin cascade and the role of different mediator molecules.

The group is integrated in European research networks (COST Action B17) and conducts a large number of collaborative projects, including cooperation with Prof. Shlomo Sasson (Jerusalem) supportet by the German-Israeli-Foundation for Scientific Research and Development.