Published in

American Diabetes Association, Diabetes, Supplement_1(67), 2018

DOI: 10.2337/db18-1889-p

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Relating Disinhibited Eating Behaviors to Resting State Functional Connectivity in Young Children

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

The prevalence of obesity among children in the United States is alarming, with recent work implicating disinhibited eating behaviors (DEBs) as a potential pathway toward obesity development. DEBs have been documented among young children, and are associated with longitudinal weight gain. However, the underlying neurobiology of DEBs in young, healthy weight children, prior to obesity development, remains unknown. This study investigated the relationship between DEBs and intrinsic neuronal connectivity in young children. We tested the hypothesis that greater DEBs would be positively associated with higher neuronal connectivity in the default mode network (DMN) and the salience network, and lower connectivity in the executive control network. The Eating in the Absence of Hunger paradigm was implemented to measure DEBs, with post-lunch calories consumed from highly palatable foods used as our main predictor. Resting state functional magnetic resonance imaging was used to examine neuronal connectivity within the networks of interest. Eighteen typically developing, healthy weight children (mean age = 5.8 years; BMI z-score = -0.6) were included in this analytic sample. Independent component analysis was used to isolate brain networks of interest. Associations between calories consumed and the three networks of interest were examined with second-level general linear models. A significant positive association was observed between calories consumed and functional connectivity in anterior cingulate cortex, a major anterior DMN hub (ACC; x=-6, y=14, z=41; t=5.23; p < 0.01, corrected). No other associations were significant. While preliminary, our results are consistent with previous studies in adults relating both DEBs and obesity status to altered neuronal response in the ACC. Our data suggest that aspects of the neurobiology of DEB are detectable in young, healthy weight children, providing a potential tool to better understand the development of obesity in this population. Disclosure A.L.B. Shapiro: None. S.L. Johnson: None. B. Mohl: None. G. Wilkening: None. K.T. Legget: None. D. Dabelea: None. J.R. Tregellas: None.