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These 2 genetic variants could impact your obesity risk


Researchers have found two rare genetic variants that could significantly increase a person's risk of becoming obese in adulthood, according to a study published Thursday in Nature Genetics.

Study details

For the study, researchers from the Medical Research Council (MRC) at the University of Cambridge looked at data from more than 500,000 people from the UK Biobank database. They found variants in two genes called BSN (also known as "Bassoon") and APBA1 that could increase a person's risk of obesity in adulthood.

Specifically, the researchers found that the variants in the BSN gene increase a person's risk of adult obesity by as much as six times, while variants in the APBA1 increase obesity risk at an "only nominally significant" rate, according to the study.

The researchers also found that the variants in the BSN gene — which affect around 1 in 6,500 adults — were associated with a higher risk of developing type 2 diabetes and nonalcoholic fatty liver disease. The variants weren't associated with childhood obesity, marking one of the first genes linked only to adult obesity, according to the study.

Discussion

The researchers hypothesized that the BSN and APBA1 genes affect obesity because they transmit signals through brain cells and can also contribute to diseases like Alzheimer's and multiple systems atrophy, which lead to brain degeneration.

As a result, it's possible that the genes play a role in damaging cells as the brain ages and removing "some of the key circuits within the brain controlling food intake and therefore you end up with obesity," according to Giles Yeo, a professor at the MRC Metabolic Diseases Unit and a co-author on the study.

According to Yeo, the findings "give us a new appreciation of the relationship between genetics, neurodevelopment, and obesity."

Yeo added that the BSN variant could eventually help drugmakers develop preventative medicines. However, the main question to answer would be, "can we actually slow down the process, prevent the process from happening to begin with, so that then we prevent more people from ending up with obesity, particularly in adulthood," he said.

John Perry, a co-author of the study and MRC investigator, said the findings "represent another example of the power of large-scale human population genetic studies to enhance our understanding of the biological basis of disease."

"The genetic variants we identify in BSN confer some of the largest effects on obesity, type 2 diabetes and fatty liver disease observed to date and highlight a new biological mechanism regulating appetite control," he added. (Furlong, Bloomberg, 4/4; Johnson, Forbes, 4/4; Massey, The Independent, 4/4)


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