Washington, Mar 13 : The team of researchers led by an Indian scientist at Ohio State University made a breakthrough in the attempts to treat obesity by creating a mouse model with characteristics suggesting that protein deficiency can lead to faster fat burning.
They believe that using a medication to manoeuvre a specific protein in humans could emerge as a strategy to treat obesity and disorders such as diabetes and metabolic syndrome.
They created the hybrid by traversing the mice deficient in protein kinase C beta (PKCB) with the C57 black mouse, a common animal used in research for studying diabetes and obesity.
"These animals can eat more than normal. And they have less fat than normal. That's a dream come true if it can be extended to human beings," said Kamal Mehta, senior author of the study and a professor of molecular and cellular biochemistry at Ohio State University.
The new mice lost weight while eating up to 30 percent more food than other mice.
"This means their lower weight was not caused by less eating, suggesting the protein deficiency corrected for the obesity tendencies by increasing the hybrids' ability to burn fat," said Mehta
The new hybrid mice developed were found to be smaller and leaner. It even had less fat distribution in the skin itself and less fat tissue overall
They also had less fat in their livers and muscles. The fat cells they did have were smaller than fat cells in other mice.
"The bottom line is we were the first to show that this deficiency leads to a lean animal. The next question is why," Mehta said.
"In order to answer why, we need to know which genes are changed in these knockout animals," he said.
The scientists also found that the new hybrid mice had more mitochondria, major source of energy for cells, within their cells than the 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.
They are conducting further studies to examine the effect of PKCB deficiency in animals.
Further studies are required 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.
"So we need to find which specific tissue needs the deficiency. Once we know which tissue is crucial for this, we can target that," said Kamal Mehta
"The whole idea is to be able to develop a drug that would safely create this deficiency in humans," he added.
However he also said that an appropriate therapy for humans would take years to develop.