Genes that increase obesity risk also can protect against diseases

Credit: CC0 Public Domain

In a new study, researchers found a range of genes that are linked to both elevated levels of body fat, as well as offering protection from some of the negative health impacts of obesity.

The findings shed new light on the biology that may disconnect a higher level of body fat from a higher risk of diabetes and heart disease.

The research was conducted by scientists at the University of Copenhagen and elsewhere.

People living with obesity tend to have unhealthy glucose and lipid levels in their blood, as well as high blood pressure.

As a result, they are more at risk of cardiovascular and metabolic diseases.

But previous research has shown that up to 45% of people living with obesity have healthy blood pressure and glucose and lipid levels, and therefore may not be at high risk of disease.

The reason why this group of people with obesity remain healthy has been poorly understood.

In the study, the team analyzed data from hundreds of thousands of people who had been assessed for their body fat and disease risk markers.

They identified 62 sections of the genome that were strongly linked to both high levels of body fat and lower risk of cardio-metabolic diseases.

Further analyses showed that the genes had a range of functions in the body, including the regulation and development of fat cells, distribution of body fat, as well as energy regulation and inflammation.

According to the team, this new knowledge is a step toward a more nuanced approach to treating obesity.

Clearly, obesity is a complex disease and not every individual with excess body weight is equally at risk of developing heart-metabolic diseases.

Knowing which genes protect people from developing diabetes and heart disease will eventually help doctors better diagnose and treat obesity.

One author of the study is Associate Professor Tuomas Kilpeläinen.

The study is published in Nature Metabolism.

Copyright © 2021 Knowridge Science Report. All rights reserved.