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Sebastian Barg’s lab published paper in prestigious The Journal of Clinical Investigation

2017-05-15

The JCI in one of the top journals in the “Medicine, Research & Experimental” category. In a recently published online article "Ca2+ channel clustering with insulin-containing granules is disturbed in type 2 diabetes", MCB researchers find that a mislocalized calcium channel causes insulin secretion defect in diabetes.

Superresolution image
showing single molecules of
calcium channels from a live
β-cell.

After a meal, the blood sugar rises. To counteract this and to make the sugar available to the body, specialized cells in the pancreas get activated to secrete insulin. In people with diabetes this mechanism fails, which leads to elevated blood sugar and a host of other diabetes related complications. The cellular signal for insulin secretion is an influx of calcium, which triggers the release of small hormone-containing storage vesicles. Recent work from Sebastian Barg’s lab at Uppsala University, in collaboration with researchers from Padua, Oxford, and the NIH, now indicates that a tiny change in the cells’ architecture is at the heart of the secretion defect. Using high resolution microscopy, the group found that calcium normally enters right next to the storage vesicle to trigger insulin release. In type-2 diabetes, the channel proteins that allow calcium the entry are instead located too far away from the insulin vesicles, which causes secretion to fail. The findings offer a first glimpse at the intricate relationship between the insulin secretion machinery and calcium channels, and suggests that drugs aimed at their interaction could be developed to treat diabetes.

These findings will be published in the June issue of the Journal of Clinical Investigation.

More information:
Article in the JCI.
Sebastian Barg's research at MCB


For more information, please contact, Sebastian Barg

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