The most prominent effect the scientists have been able to identify so far relates to the mitochondria, the principal energy source of cells. Mehta said the new hybrid mice have more mitochondria within their cells than do normal mice, and that the added energy source allows them to convert fatty acids into energy.
We have shown to some extent that there is increased fatty acid oxidation. We found that they use more oxygen, so that means they are using this oxygen to metabolize fat, convert it into carbon dioxide and expel it when they breathe, said Madhu Mehta, a clinical consultant and co-author on the study and assistant professor of internal medicine at Ohio State.
The research group is testing this finding with an additional experiment, introducing the PKCB 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 diabe
|Contact: Kamal Mehta|
Ohio State University