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Old Wed, Oct-14-20, 12:06
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Demi Demi is offline
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Default Obesity risk linked to gene that drives inflammation

Obesity risk linked to gene that drives inflammation

Ottawa scientists have found a link between a gene involved in tissue inflammation and obesity that offers new hope for people who suffer from the complex disease.

The study, recently published in the journal Nature Metabolism, established that elevated levels of the molecule RIPK1 – it plays a role in driving inflammation in the body – predispose people to obesity. Scientists found that people with mutant copies of the gene that expressed RIPK1 were more likely to be obese.

For years, scientists have understood that obesity causes inflammation, but this is the first time that they’ve proven the reverse is also true: that a gene involved in inflammation causes obesity.

“Our work here is significant because it proves for the first time that an inflammatory factor predisposes people genetically to obesity,” said Dr. Katey Rayner, director of the cardiometabolic microRNA laboratory at the University of Ottawa Heart Institute.

Rayner, principal investigator of the study, said heart disease and obesity share a number of risk factors and mechanisms.

Eating too much creates an immune response in the human body, which in turn triggers the kind of inflammation that has been tied to a number of chronic diseases, including arthritis and heart disease.

Scientists have, for years, understood that obesity has a genetic component: that genes related to appetite control and metabolism – the way that calories are processed by an individual – can be inherited.

Rayner said the discovery of RIPK1’s role in obesity will give scientists a whole new avenue to explore for potential treatments.

“There are things in our genes that we can’t control and that are affecting our biology: this is one of them,” Rayner said. “From a therapeutic perspective, it gives a whole new biology to target for obesity. It’s not appetite and it’s not calories.”

Rayner’s lab proved the association between RIPK1 and obesity through a genetic analysis of people with obesity and a study that examined what happens when the gene is turned off in mice.

Researchers found elevated levels of the RIPK1 gene in the fat tissue of obese people, and further analysis showed that people with a mutant copy of the gene tended to be more obese. About 8 to 12 per cent of the poplulation have variations in the RIPK1 gene.

When researchers gave mice a drug that blocked the expression of RIPK1, the mice remained at a normal weight even though eating a high-carlorie diet. Their risk of diabetes was also reduced.

The treatment had no effect on the lean body mass of the mice.

“I think the most exciting thing from the average person’s perspective is that these mice were able to continue to eat and act how they wanted – and they still did not gain weight,” said Rayner.

Rayner, however, cautioned that it’s unlikely that scientists will be able to develop a single pill that will allow people to eat as much as they want without the need to exercise.

“For sure, this is not going to be a complete magic bullet,” she said. “But for the person who is doing all the other things to combat obesity and all its complications, this will hopefully give them a completely separate way to do it, and add it on top of all the other things we have to curb obesity.”

Obesity is known to increase the risk of other health problems, including heart disease, diabetes, arthritis, high blood pressure and some cancers. According to Statistics Canada , almost 27 per cent of Canadian adults – about 7.3 million people – can be classified as obese based on their height and weight.

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