Dr. Erik Renstroem

VGCCs in pancreatic islets and their role in diabetes.

Lund University, Sweden

The Unit for Islet Pathophysiology at the Department of Clinical Sciences at Lund University focuses on identifying the mechanisms for defective insulin secretion that cause or accelerate human type 2-diabetes. This research focus necessitates a front-line experimental repertoire in cell biology, as well as integration with clinical and genetic research groups. Currently there are 3 permanent academic staff, 12 post-docs, 7 PhD students and 3 technicians. Our unit has an excellent track record in diabetes research with numerous publications in top journals, using electrophysiology, live cellular imaging (confocal, TIRF & multiphoton), molecular biology approaches (e.g. viral gene transfer and RNA interference) in combination with in vivo investigations. Recently, we have shed new light on the how normal biphasic insulin secretion is generated; fundamental knowledge for understanding why this process fails in early diabetes. We have demonstrated that rapid 1st phase insulin secretion is evoked by L-type CaV1.2 channels, whereas sustained late phase secretion is controlled by R-type CaV2.3 channels.We have also elucidated insulin granule trafficking, which occurs by a combination of random and directed movement and myosin-Va-driven granule transport. These processes are affected by 2nd messengers and metabolites; we recently demonstrated a redox control of insulin release by the pyridine nucleotide NADPH . Effects of NADPH on ion channel activity is currently being investigated.

We also operate in a strong environment: a constellation of diabetes researchers, in which our unit plays a vital role, were awarded a Strategic Research Centre in December 2005 by the Swedish Foundation for Strategic Research ( Furthermore, this consortium has also been short-listed for long-term support in an ongoing initiative from the Swedish Research Council (Linnaeus grants).

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L-type calcium channels in health and