Researchers have identified a genetic mutation strongly associated with childhood obesity, which could ultimately enable the development of new treatments.
- The scientists more specifically studied a variant of the chr12q13 locus harboring the FAIM2 gene, which is more linked to childhood obesity.
- The variant is an allele called rs7132908 which is present in the hypothalamus.
- This decreases FAIM2 levels and, during childhood, prevents the development of neurons that help regulate appetite.
Since 1990, adolescent obesity has quadrupled according to the World Health Organization (WHO). Among children and adolescents aged 5 to 19, 160 million are obese worldwide. The main reason is too rich a diet and low physical activity, indicates theHealth Insurancewhich also emphasizes that psychological, genetic factors and even chronic illnesses can promote weight gain.
Focusing on the “chr12q13” locus which is more linked to childhood obesity
In a new study published in the journal Cell Genomics, researchers have identified a genetic mutation strongly associated with childhood obesity. To fully understand it, we must take stock of the current state of knowledge, on which researchers have relied.
Neural pathways in the hypothalamus have previously been shown to control appetite and therefore may be regulators of disease. In addition, researchers have also identified specific genetic markers – locus – linked to obesity. But their mechanisms were difficult to study.
During their work, the scientists more specifically studied chr12q13, a locus harboring the FAIM2 gene, which is more linked to childhood obesity. “By focusing specifically on this locus, we were able to identify a mutation present in one of the genetic signals most involved in childhood obesity”indicates Sheridan H. Littleton, one of the authors, in a communicated. In addition to being associated with obesity, the locus was linked to other health problems such as type 2 diabetes, early menstruation or even a higher percentage of body fat.
The allele associated with obesity risk influenced the expression of the FAIM2 gene
In a second step, the scientists studied a variant of this locus, a allele called rs7132908, present in the hypothalamus and linked to the risk of obesity. To do this, they analyzed stem cells from neurons present in this area. Thus, they discovered that the allele associated with obesity risk had two impacts. He decreases FAIM2 levels. Furthermore, theNeurons with the rs7132908 allele were less likely to transform and help regulate appetite.
An imbalance in appetite-stimulating neurons
According to the authors, lower levels of FAIM2 during a period in childhood could lead to an imbalance between appetite-stimulating and appetite-suppressing neurons. Over time, this could result in a propensity to overeat and gain weight.
There are therefore children who are genetically more at risk of gaining weight. However, scientists emphasize that this variant does not condemn the child, who can avoid obesity with a balanced diet and the practice of physical activity.
“This work highlights how the brain plays a central role in the genetics of obesity and provides us with a strategy for further study”, says Dr Struan FA Grant. Ultimately, this discovery could therefore enable the development of new treatments against obesity, by specifically targeting the action of this genetic mutation.
