Adolescents at high risk of obesity show greater striatal response to increased sugar content in milkshakes

Abstract

Background: Children of overweight or obese parents are at a high risk of developing obesity.

Objective: This study sought to examine the underlying neural factors related to parental obesity risk and the relative impact of sugar and fat when consuming a palatable food, as well as the impact of obesity risk status on brain response to appetizing food images.

Design: With the use of functional MRI, the responses of 108 healthy-weight adolescents [mean ± SD body mass index (kg/m2): 20.9 ± 1.9; n = 53 who were at high risk by virtue of parental obesity status, n = 55 who were low risk] to food stimuli were examined. Stimuli included 4 milkshakes, which systematically varied in sugar and fat content, a calorie-free tasteless solution, and images of appetizing foods and glasses of water.

Results: High-risk compared with low-risk adolescents showed greater blood oxygen-dependent response to milkshakes (all variants collapsed) compared with the tasteless solution in the primary gustatory and oral somatosensory cortices (P-family-wise error rate < 0.05), replicating a previous report. Notably, high-risk adolescents showed greater caudate, gustatory, and oral somatosensory responses to the high-sugar milkshake than to the tasteless solution; however, no effect of risk status was observed in the high-fat milkshake condition. Responses to food images were not related to obesity risk status.

Conclusion: Collectively, the data presented here suggest that parental weight status is associated with greater striatal, gustatory, and somatosensory responses to palatable foods-in particular, high-sugar foods-in their adolescent offspring, which theoretically contributes to an increased risk of future overeating. This trial was registered at www.clinicaltrials.gov as NCT01949636.

Figures

FIGURE 1

No difference in BMI was seen between the high- and low-risk groups (n = 53 and 55, respectively) at baseline (P = 0.28) (A). There was a significant difference in BMI at the 3-y follow-up visit as a function of obesity risk status: high- compared with low-risk participants (n = 42 and 46, respectively) had a significantly higher BMI (*P = 0.002) (B). Values are means ± SEs. Post hoc 1-factor ANOVA was used to assess risk-dependent differences in BMI at the year 3 follow-up; Tukey’s honestly significant difference test was used to correct for multiple comparisons.

FIGURE 2

Greater response in the left anterior insula (MNI coordinates 46, −4, −2; z score = 2.99, P-FWE = 0.04, k = 30) (A) and the left orbital frontal cortex (MNI coordinates 40, 22, 8; z score = 4.07, P-FWE = 0.03, k = 257) (B) in the high-risk group (n = 53) compared with the low-risk group (n = 55) during receipt of all 4 milkshakes compared with a tasteless solution. Greater activation in the left caudate (MNI coordinates 10, 10, 14; z score = 3.68, P-FWE = 0.03, k = 11) (C) and the left central operculum (MNI coordinates 44, 8, 6; z score = 3.86; P-FWE = 0.04, k = 40) (D) in the high-risk group (n = 53) compared with the low-risk group (n = 55) during receipt of the high-sugar and low-sugar milkshake compared with a tasteless solution. Bar graphs represent mean PEs extracted from the local peak response denoted by the cross-hairs; error bars denote SDs. P values and clusters were generated by using threshold free cluster estimation through FSL's randomize (version 5.0.9, Functional Magnetic Resonance Imaging of the Brain group) with the use of a 2-sample t test. Local maxima were calculated with FSL's cluster tool. Coordinates are presented in MNI space. FWE, family-wise error rate; MNI, Montreal Neurological Institute; PE, parameter estimate.