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UCSF discovers new glucose-regulating protein linked with diabetes
Date:5/28/2009

ls fail to respond appropriately to the insulin and the GLUT4 compartment is abnormal. This process was thought to be identical across mammal species.

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

The team determined that this protein is a specialized form of a ubiquitous housekeeping protein called clathrin, which Brodsky has studied since the 1980s and is known to be instrumental in moving proteins between cellular compartments. CHC22 was observed to be associated with the abnormal GLUT4 compartments in muscles from diabetic patients which, for some reason, do not mobilize to the muscle cell surface when stimulated by insulin.

Notably, she said, while mice also have an insulin-responsive GLUT4 compartment, they lack the CHC22 protein. As a result, this work has implications for developing better models for the study of type 2 diabetes.

The paper highlights the differences between humans and mice and offers insights into aspects of the GLUT4 transport mechanism within cells that are specialized in humans, according to a commentary on the paper that appears in the same journal.

Brodsky said the Harvard team on this research produced the mouse capable of expressing CHC22 in its muscles and fat, which was analyzed in the study. These mice have features of diabetes, because the protein disrupts their GLUT4 transport pathway, which normally operates without CHC22. Also instrumental to the study was a human muscle cell line produced by the collaborator at University of Texas Southwestern.


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Contact: Kristen Bole
kbole@pubaff.ucsf.edu
415-476-2557
University of California - San Francisco
Source:Eurekalert

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