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deficiency to animals with a lower production of mitochondria to see if the level of mitochondria
increases when the protein is not present.
More work also needs to be done to determine whether the protein could be deficient in just certain
types of cells to produce the same effect ­ for example, by eliminating the protein from only liver
cells or fat tissue cells rather than throughout the body. Under current circumstances, the deficiency
is present in the entire mouse genome.
"So we need to find which specific tissue needs the deficiency. Once we know which tissue is
crucial for this, we can target that," Kamal Mehta said. "The whole idea is to be able to develop a
drug that would safely create this deficiency in humans."
Mehta also is leading a study testing the effect of PKCB deficiency on diabetes in particular,
examining whether the disease can be prevented by the elimination of this protein. An excess of
triglycerides in tissue can lead to insulin resistance, a hallmark of diabetes. Because the protein
relates to how the body burns triglycerides, Mehta believes the deficiency also could play a role in
preventing the disease from developing.
The deficiency does not appear to pose any health problems. The mice with the deficiency lived a
normal lifespan and experienced no premature deaths.
It remains unknown whether the deficiency currently exists naturally in humans. "Genetic testing of
lean people could help answer that question," Mehta said.
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This research was supported by the National Institutes of Health.
Co-authors on the study were Rishipal Bansode, Wei Huang and Sanjit Roy of the Department of
Molecular and Cellular Biochemistry and the Davis Heart and Lung Research Institute.
Contact: Kamal Mehta, (614) 688-8451;
Written by Emily Caldwell, (614) 292-8310;


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