A new study found that the lipid transporter gene that increases risk to diabetes among Mexicans and other Latin Americans is also present in the Neanderthal gene. The gene is believed to be formed when modern humans interbred with the Neanderthals.
Researchers from the Slim Initiative in Genomic Medicine for the Americas Type 2 Diabetes Consortium (SIGMA) compared the genes of Mexicans and Latin Americans with the non-Hispanics to find out which ethnicity carries the most number of genes linked to type 2 diabetes.
They analyzed a total of 9.2 million single nucleotide polymorphisms (SNPs) from more than 8,000 participants. About 48 percent of the group was diagnosed with type 2 diabetes. However, they also examined those were free from the disease.
Their analysis identified two carrier genes, SLC16A13 and SLC16A11, which are present on those with type 2 diabetes. The association seemed to be stronger among younger and leaner people who have diabetes and this was replicated in other sampling done independently.
The SLC16A11 gene variant is believed to be a product of the Neanderthals interbreeding with modern humans. This belief is still being studied by scientists.
Each gene variant increases risk by around 20 percent which means that a person carrying both variants will have an elevated risk by up to 40 percent. The risk of inheriting type 2 diabetes is doubled when both parents were carrying the two variants. Researchers found that most Latin Americans and Mexicans are already carriers of the SLC16A13 and SLC16A11.
The researchers also looked at other ethnicities for comparison. They found that 50 percent of the modern Native Americans were carriers while it was only 10 percent on the East Asian and African populations. Modern Europeans rarely have the carrier genes.
This new study is expected to contribute to the understanding of diabetes and help improve the assessment of risk factors to deliver new drug targets. It also outlines the importance of risk genes identification among understudied populations to increase knowledge of the pathophysiology of a disease.
The study was published in the December 25 issue of Nature.
