New research findings from MCB


Type-2 diabetes - insulin is held up in traffic

Researchers at the Dept of Medical Cell Biology and at Lund University discover that vesicle traffic is defective in human type-2 diabetes, leading to decreased insulin secretion.

Type 2 diabetes is a major public health issue with globally more than 400 million individuals affected. Both lifestyle and hereditary components contribute to the disease. The main problem is insufficient secretion of the blood glucose-lowering hormone insulin, which is produced by β-cells within the pancreas and secreted into the bloodstream after a meal. New research from the Dept of Medical Cell Biology indicates that this is due to a defect that slows down the traffic of insulin packages out of the β-cell. Insulin is released when small insulin-containing vesicles fuse with the cell membrane, which ejects the hormone into the bloodstream. For this to happen, each of the vesicles must first attach to the cell membrane and allow its secretion machinery to be assembled. By comparing β-cells from healthy and type 2 diabetic individuals, the team led by Sebastian Barg found that the problem lies in the attachment of the insulin vesicles to the cell membrane. In diabetic β-cells, arrival of new vesicles at the cell membrane is dramatically slowed, which is likely due to a reduction in several of the proteins responsible for their attachment at the cell membrane. As a consequence, new insulin vesicles cannot assemble their secretion machinery and the amount of insulin that reaches the body is insufficient. The hope is now that the report, which was published in the journal Cell Metabolism, can guide the development of new treatments for type-2 diabetes.

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Read more about Sebastian Barg's research.