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Oct 6, 2020 // -- In a recent study published in the international journal Nature Metabolism, scientists from the University of Queensland and others found that a specific gene that helps control inflammation in the body may increase the risk of obesity in individuals, effectively blocking weight gain in mice after being turned off for expression.
: In the CC0 Public Domain study, researchers wanted to reveal a link between inflammation and obesity, not overealing or lack of exercise.
researcher Karunakaran said: 'We found small changes in the inflammatory gene RIPK1 in obese people that increase the level of gene expression in adipose tissue, which in turn increases an individual's risk of obesity.'
RIPK1 is critical to the body's healthy immune response, but when it goes wrong, it induces an excessive inflammatory response, and when researchers find an increase in inflammatory levels in obese people, they can be sure that obesity does induce inflammation.
The researchers then looked at the effects of the expression of the inflammatory gene in mice, without the RIPK1 gene, which maintained a normal weight despite a high-fat diet and reduced the risk of diabetes in mice, while mice with normal levels of RIPK1 showed weight gain after eating the same high-fat diet.
researchers say that more than half of the 2,000 participants showed extreme obesity, with an average BMI of 41, and half of them showed normal body weight;
'By understanding a variety of inflammatory pathfages, we may be able to find specific ways to treat obesity, especially in particular obese people, where mutations in the RIPK1 gene occur only 8 to 12 percent of the population, so later researchers may use it as a target to develop new strategies to combat obesity,' said Katey Rayner, a researcher at the end of the study.
() Original source: Karunakaran, D., Turner, A.W., Duchez, A. et al. RIPK1 gene variants associate with obesity in humans and can be therapeutically silenced to reduce obesity in mice. Nat Metab (2020). doi:10.1038/s42255-020-00279-2.