ESPE Yearbook of Paediatric Endocrinology

Brief summary: Roth et al. studied the relationship between obesity outcomes and meal-induced changes in neural activation to high- versus low-calorie food cues before and after 24-week family-based behavioral treatment (FBT) in n=28 children (9–11 years) with obesity and in n=17 children of healthy weight without intervention (9–11 years). Among children with obesity who underwent FBT, unfavorable changes were observed in peripheral hormone secretion after weight loss and also a weaker satiety response.

It is still poorly understood why there are rates up to 50% of unresponsiveness, and why many children regain weight shortly after ending familial-based behavioral treatment (FBT). This study is one of the first to assess the interplay between neuroendocrine factors with obesity treatment in children. It studied the effect of an obesity intervention on changes in central and peripheral satiety signaling in response to a meal. One of the main findings was that in children with obesity who underwent FBT, a greater reduction in BMI z-scores was associated with developing a weaker central satiety response to a meal from before to after FBT. This could predispose children to overeating and weight regain after FBT. These observations support the hypothesis that in the presence of weight loss the brain defends elevated body weight (1), even in young children.

This study and others have also shown that an FBT intervention and weight loss lead to meaningful change of peripheral satiety-regulating hormones (2,3), but Roth et al. observed at the same time a weaker central response to a meal. This could mean that even when peripheral satiety responses by gut hormones are intact among children with obesity who are successful in FBT, their central regulation of satiety is disturbed. Long-term lifestyle and behavioral interventions or pharmacological approaches are required to intervene on the obesity-related set point that strongly defends higher body weight.

References: 1. Schwartz MW, Seeley RJ, Zeltser LM, Drewnowski A, Ravussin E, Redman LM, Leibel RL. Obesity pathogenesis: an endocrine society scientific statement. Endocr Rev 2017;38:267–296. doi: 10.1210/er.2017-00111. 2. Jensen DE, Nguo K, Baxter KA, Cardinal JW, King NA, Ware RS, Truby H, Batch JA. Fasting gut hormone levels change with modest weight loss in obese adolescents. Pediatr Obes 2015;10:380–387. doi: 10.1111/ijpo.275. 3. Reinehr T, Roth CL. The gut sensor as regulator of body weight. Endocrine 2015;49:35–50. doi: 10.1007/s12020-014-0518-1.