The second JAMA Pediatrics paper, in collaboration with King's College London, sheds further light on the way that appetite, particularly low satiety responsiveness, acts as one of the mechanisms underlying genetic predisposition to obesity.
The researchers accessed data from 2,258 10-year-old children born in the UK between 1994 and 1996. The team created a polygenic obesity risk score (PRS) for each child to estimate their genetic susceptibility to obesity, by adding up the number of higher-risk alleles from 28 obesity-related genes. Higher PRS scores indicated a higher genetic predisposition to obesity.
The PRS scores were then examined to determine the correlation with the children's satiety responsiveness and adiposity (body fatness).
"As expected, we found that children with a higher PRS score (more obesity-risk' genetic variants) were likely to have larger BMI and waist circumference," says Dr Clare Llewellyn, lead author from the UCL Health Behaviour Research Centre. "But more importantly, we also found that these children were more likely to have low satiety responsiveness.
"This suggests that satiety sensitivity could be targeted for pharmacological and behavioural interventions, to prevent or treat obesity. For example, children with lower satiety sensitivity could be taught techniques that might improve their fullness signals when eating, such as slowing their eating speed. Another approach might be to provide better advice to parents and children about appropriate portion sizes, limiting access to 'second helpings' and ensuring tempting treats are out of sight between meals."
|Contact: David Weston|
University College London