New Glucose-Regulating Protein Linked With Diabetes Identified

A specialized protein in human muscles is linked with the process that clears glucose out of the bloodstream, scientists have revealed.

The finding by researchers at the University of California, San Francisco, and collaborators at Harvard Medical School, could shed light on what goes wrong in type 2 diabetes on a cellular level.

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If the function of this protein (apparently absent in mice) is established, it could pave the way for future study and possible therapies for diabetes.

"Much has been learned from mouse models about glucose metabolism that is relevant to human diabetes, but what happens on a cellular level is now found to be different between the two species. This research shows one significant species-specific difference that will influence our understanding of mechanisms of type 2 diabetes," said Dr. Frances Brodsky, senior author on the paper.

The researchers said that in humans, muscles play a key role in clearing glucose from the bloodstream-a process normally controlled by insulin, which stimulates the muscle cells to import glucose by means of a system known as the GLUT4 glucose transporter.

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Usually GLUT4 is stored inside both human and mouse muscles in a special compartment that releases it upon insulin stimulation. Fat cells also form a GLUT4 compartment and take up glucose in response to insulin.

But, in type 2 diabetes, the muscle and fat cells fail to respond appropriately to the insulin and the GLUT4 compartment is abnormal-a function thought to be identical across mammal species.

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The current research identified a protein in both human muscle and fat cells-called CHC22-that appears to control the formation of the GLUT4 storage compartments.

The team determined that this protein is a specialized form of an omnipresent housekeeping protein called clathrin, which is known to be instrumental in moving proteins between cellular compartments.

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The researchers observed that CHC22 was associated with the abnormal GLUT4 compartments in muscles from diabetic patients, which, for an unknown reason, do not mobilize to the muscle cell surface when stimulated by insulin.

She particularly said that while mice have an insulin-responsive GLUT4 compartment, they lack the CHC22 protein.

Thus, this work has implications for developing better models for the study of type 2 diabetes.

The study has been published in the journal 'Science'.

Source-ANI
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