Obesity gene

As the obesity epidemic in children and adults continues across North America, researchers continue to study exactly what is causing it.

Of course we can point to lifestyle factors such as diet and exercise as obvious culprits in some cases. Sedentary lifestyles, fast food and urban sprawl are all important issues worthy of attention and solutions as well as ensuring food security and variety in isolated and lower income communities.

Still – we likely all know individuals who seem to do everything right on the lifestyle front yet continue to struggle with obesity.

Researchers at the Max Planck Institute of Immunobiology and Epigenetics in Freiberg Germany have discovered something that works like a genetic light switch – causing one person to deal with a lifetime of obesity while their identical twin could maintain normal weight.

What this means is for many people obesity may not be caused by inherited traits or lifestyle factors such as over-eating. Rather, according to researcher Andrew Pospisilk, obesity can be triggered in the womb or in early childhood by an unknown factor.

Pospisilik and his colleagues study epigenetics – how genes can change their function or be ‘switched’ on or off due to environmental conditions.

His study examined genetically identical mice with a mutation in a gene protein called Trim28. Some of the mice grew to normal weight while others became obese. It seemed something triggered a change in the gene expression in some but not others.

The same researchers continued and found a similar result in children with the same mutation. Further, the very same result showed up when the researchers examined medical information from sets of identical twins in which one was normal weight and other obese.

In all cases, Trim28 activity was suppressed in the obese individuals but not in those of normal weight.

It is not yet understood what triggers the change in gene expression for some and not others or at what point in life it happens. Pospisilik suspects it occurs during gestation in mice – but it could be different for humans since human brain development continues throughout childhood. Discovering why and when it occurs will be the focus of research going forward.

One optimistic point of note is that in mice the gene appears to reset in each generation meaning that a parent with the obesity expression of the gene will not necessarily have obese children.

I look forward to hearing more updates from this research group. If we could pinpoint its cause and learn how to prevent or reverse the mutation from occurring, we could alleviate a significant burden on people’s health and the health care system.

 

 

 

 

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