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Removing DNA repair gene causes metabolic syndrome

to restore DNA to its undamaged state.

"Our analysis is that the inability to repair damage to the genetic material, whether it is in the nucleus or whether it's in the mitochondria, is what's leading to a destabilization of a normal metabolic process," Lloyd said. "That then begins to cascade and ultimately results in the symptoms that are consistent with the metabolic syndrome."

Lloyd says he hopes to study individuals suffering from the metabolic syndrome with the goal of someday developing a genetic screen for the disease. He also wants to examine ways to delay the onset of symptoms, such as increasing the expression of the NEIL1 gene or dampening oxidative stress to the cells that damages their DNA. Such techniques could one day become therapies.

"One may be able to develop a diagnostic method to do early screening," Lloyd said. "Or there could be a drug discovery mechanism in which you enhance the transcription process (of NEIL1) and just make more. Maybe you only have one good copy. Fine. Maybe we can upregulate that one."

More importantly, "What we think this publication is going to do is add one more complexity to the potential mechanisms by which you could get to disease," he said.


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Source:Oregon Health & Science University


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