During the development of type 2 diabetes, uptake of glucose from the blood by muscle and fat cells in response to insulin is reduced. The pathways involved in the insulin-stimulated uptake of glucose were believed to be similar in all mammals, but US scientists have now highlighted a key difference between mice and humans. Glucose is taken up by fat and muscle cells via the GLUT4 glucose transporter, thus removing glucose from the bloodstream. When blood glucose is low, the receptor is sequestered away from the cell surface and is released from the intracellular compartment in response to insulin stimulation when blood glucose rises. In type 2 diabetes, however, the GLUT4 compartment is abnormal and the transporter is not mobilised to the cell surface in response to insulin stimulation. The muscle isoform of clathrin heavy chain, CHC22, was found to be involved in formation of the intracellular GLUT 4 components in human muscle cells and adipocytes and was also found to be associated with the abnormal GLUT4 compartments in muscle cells from people with type 2 diabetes. Mice also have an insulin-responsive GLU4 compartment but lack the CHC22 protein – mice engineered to express CHC22 in fat and muscle tissue had defects in their GLUT4 transport pathway and showed features of diabetes, including high blood sugar and reduced responses to insulin. As well as suggesting that faulty vesicle trafficking, as well as problems with insulin signalling, may play a role in the development of type 2 diabetes, the study highlights the importance of being aware of differences between animals used in model studies and humans.
The study is published in the journal Science.
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[...] a previous post we reported on a study that shows that mice may not be a good model for human diabetes. A new study [...]