An analysis of the genomes and epigenomes of lean and obese mice and humans has turned up a wealth of clues about how genes and the environment conspire to trigger diabetes, Johns Hopkins researchers say. Their findings reveal that obesity-induced changes to the epigenome—reversible chemical "tags" on DNA—are surprisingly similar in mice and humans, and might provide a new route to prevention and treatment of the disease, which affects hundreds of millions worldwide. A report on the study appears Jan. 6 in the journal Cell Metabolism.
"It's well known that most common diseases like diabetes result from a combination of genetic and environmental risk factors. What we haven't been able to do is figure out how, exactly, the two are connected," says Andrew Feinberg, M.D., M.P.H. , Gilman Scholar and director of the Center for Epigenetics in the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine. "This study takes a step in that direction."
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