The most common genetic cause of severe obesity in children is a condition called “MC4R haploinsufficiency” in which the child has one defective copy of a gene involved in food intake and metabolism (melanocortin 4 receptor or MCR4).
The findings, reported in the March issue of Endocrinology, suggest that early nutritional interventions might slow the rate of weight gain in children with this condition.
Roger Cone and colleagues are examining how dietary fat content affects feeding behavior in mice in which one or both copies of the gene are deleted. They found that diets high in either saturated or monounsaturated fats cause the genetically modified mice to eat more fatty food at a much faster rate than normal, wild mice – suggesting that fatty food is more rewarding yet less satisfying to the mice missing the receptor. They also identified alterations in lipid signaling molecules that may play a role in the increased feeding behavior.
This research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the Robert C. and Veronica Atkins Foundation, and a University Development Commission Scholarship, Ministry of University Affairs, Thailand.