Researchers at the University of California, San Francisco, and collaborators at Harvard Medical School have linked a specialized protein in human muscles to the process that clears glucose out of the bloodstream, shedding light on what goes wrong in type 2 diabetes on a cellular level.
Establishing the function of this protein, which significantly is not present in mice, has broad implications for both the future study and possible therapies for diabetes, according to an article published in the May 29, 2009 issue of the journal "Science."
While a significant amount of research into diabetes and many other diseases is conducted in mice, the often-unknown differences between mice and men can create obstacles to direct translation of such research and need to be taken into account in understanding the progression of human disease, according to the researchers.
"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," said Frances Brodsky, DPhil, senior author on the paper and a UCSF professor in the Departments of Bioengineering and Therapeutic Sciences, Pharmaceutical Chemistry, and Microbiology and Immunology. "This research shows one significant species-specific difference that will influence our understanding of mechanisms of type 2 diabetes."
In humans, muscles play a key role in clearing glucose from the bloodstream, Brodsky explained. In normal function, this is controlled by insulin, which stimulates the muscle cells to import glucose by means of a system known as the GLUT4 glucose transporter.
Normally, she said, 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. In type 2 diabetes, however, the muscle and fat cel
|Contact: Kristen Bole|
University of California - San Francisco