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Diabetes risk factor common in Latin Americans likely inherited from Neanderthals

A genetic risk factor for type 2 diabetes commonly found in the DNA of Mexican and other Latin Americans was probably inherited from Neanderthals when they interbred with humans some 50,000 years ago, according to an exhaustive new analysis.

Scientists at the Broad Institute, a Cambridge genomic research center, worked with colleagues to compare more than 9 million spots in the genomes of 8,000 Latin Americans and found a version of a gene that increased a person's risk for the disease by about 20 percent.

The research, published Wednesday in the journal Nature, was supported by Mexican billionaire Carlos Slim Helú, who visited the Broad Institute this fall to announce a $74 million gift for continued genetics research in Latin American populations.

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Mexican and Latin American people have about twice the rate of diabetes as non-Hispanic white people in the United States, leading researchers to wonder whether different genetic risk factors were at play.

They were especially intrigued by one new gene that was strongly associated with the disease when five changes were made to its DNA letters.

That version of the gene was nearly absent from African populations and rarely seen in Europeans. It was found in about 10 percent of Asians, and in about half of Native Americans, raising the suggestion that it entered the human gene pool after humans left Africa.

"We were intrigued, and it eventually dawned on us that archaic interaction" — crossbreeding with Neanderthals — "might be the source of this," said Amy Williams, a post-doctoral researcher at the Broad and Harvard Medical School. Williams and colleagues got access to a Neanderthal genome sequence and found it there, suggesting that the version of the gene entered the human population when the two species interbred.

That doesn't suggest that Latin Americans have any more or less Neanderthal DNA than others.

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The task ahead for the team now is to better understand the role the gene may play in causing the disease. Initial studies revealed that it is active in fat metabolism in the liver, and researchers at the Broad hope to understand the biology to help inform the hunt for therapies.


Carolyn Y. Johnson can be reached at cjohnson@globe.com. Follow her on Twitter @carolynyjohnson.