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Mouse with designer liver has enhanced glucose tolerance, insulin response

ated mouse strain. Interestingly, the LGKO mice had reduced blood glucose levels and lower levels of serum insulin. The mice retained triglycerides in the liver with a commensurate decrease of circulating triglycerides in the bloodstream. Insulin response to glucose load was diminished in LGKO mice, thus glucose tolerance in the liver was significantly improved in the absence of Gab1 protein.

The Feng team conducted biochemical analyses on the LGKO mice, homing in on enzymatic pathways critical to insulin response in cells. Upon stimulation with insulin, they found an elevated level of Akt/PkB kinase, an enzyme needed for insulin signaling, and elevated activity of IRS proteins. There was no activation of another enzyme, Erk, which is elevated in normal liver in reaction to insulin stimulation. Dr. Feng concluded that the function of Gab1 in normal liver cells is to promote signaling in the Erk pathway, which reduces insulin response signals flowing through IRS and Akt proteins.

"We propose that Gab1 acts as a negative regulator on insulin signal strength in the liver," said Dr. Feng. "In this work, by making a new liver-specific gene knockout mouse model, we found a novel balancing mechanism for control of liver insulin signaling. Our observation might be instrumental for understanding better the pathogenesis of type 2 diabetes and designing anti-diabetes drugs."

Co-authors on this study from Dr. Feng's laboratory were Emilie Bard-Chapeau, Ph.D., and Shinong Long, Ph.D., postdoctoral fellows, and Eric Zhang, graduate student in the Burnham Institute-UCSD's joint graduate training program in Molecular Pathology.

Jerrold Olefsky, Ph.D. and Andrea Hevener, Ph.D. are Professor and Adjunct Associate Professor, respectively, in the Department of Medicine at the University of California, San Diego.

This project was supported by grants from the National Institutes of Health awarded to Drs. Feng, Olefsky, and Hevener. Dr. Feng acknowl
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Source:Burnham Institute


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