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Correlation between food-evoked signal change in the dorsolateral frontal cortex and ad libitum food consumption: a human neuroimaging study

By: Publication details: 2016Uniform titles:
  • Diabetologia
Online resources: Summary: <span style="font-size: 10pt;">Background and aims:Mechanisms causing weight loss after Roux-en- Y gastric bypass (RYGB) are unclear. Modulation of inhibitory control of food intake may contribute. Aim: To explore correlations between brain responses to food ingestion and ad libitum food intake in normal weight (NW), obese (Ob) and post-RYGB people. Materials andmethods: Twelve NW(age 32.3+/-9.3 years,BMI 22.3+/-1.4 kg/m2), 21 Ob (age 31.1+/-10.5 years, BMI 34.1+/-2.6 kg/m2) and 9 RYGB (age 45.1+/-10.7 years, BMI 34.0+/-3.3 kg/m2) subjects underwent [18F]- fluorodeoxyglucose positron emission tomography (FDG-PET) neuroimaging twice after overnight fasting: once FED (400 kcal mixed meal before scanning), once FASTED (water only) in random order. Subjects underwent an ad libitummeal after scanning. Brain FDG uptake, amarker of neuronal activation, was compared using Statistical Parametric Mapping. In clusters showing an interaction between fed state and group (voxel level p<0.01, cluster size threshold 100 voxels), post hoc Spearman's correlational analyses between food-evoked FDG signal change (FESC, FED minus FASTED) and ad libitum consumption at the FASTED visit were performed. Results: There were 10 clusters where the response to food ingestion was different between groups (previously reported). Correlations within each group between FESC in each cluster and ad libitum consumption are shown in the table. Mean+/-SD FESCs in cluster C were: NW -4.02 +/-2.48%, Ob -0.11+/-1.22%, RYGB -4.18+/-3.07%. Conclusion: The highly significant, strong, positive correlation in NW between FESC in cluster C (DLFC) and ad libitum consumption, with greater deactivation associated with lower ad libitum consumption, supports an association between DLFC deactivation (in this FDG-PET neuroimaging paradigm) and increased inhibitory control of food intake. There were no such correlations in Ob or RYGB. The mean FESCs in cluster C are consistent with low inhibitory control of food intake in the obese which is increased after RYGB and suggest altered DLFC activity after RYGB may contribute to weight loss. (figure present).&nbsp;[Conference Abstract]</span>
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&lt;span style="font-size: 10pt;"&gt;Background and aims:Mechanisms causing weight loss after Roux-en- Y gastric bypass (RYGB) are unclear. Modulation of inhibitory control of food intake may contribute. Aim: To explore correlations between brain responses to food ingestion and ad libitum food intake in normal weight (NW), obese (Ob) and post-RYGB people. Materials andmethods: Twelve NW(age 32.3+/-9.3 years,BMI 22.3+/-1.4 kg/m2), 21 Ob (age 31.1+/-10.5 years, BMI 34.1+/-2.6 kg/m2) and 9 RYGB (age 45.1+/-10.7 years, BMI 34.0+/-3.3 kg/m2) subjects underwent [18F]- fluorodeoxyglucose positron emission tomography (FDG-PET) neuroimaging twice after overnight fasting: once FED (400 kcal mixed meal before scanning), once FASTED (water only) in random order. Subjects underwent an ad libitummeal after scanning. Brain FDG uptake, amarker of neuronal activation, was compared using Statistical Parametric Mapping. In clusters showing an interaction between fed state and group (voxel level p&amp;lt;0.01, cluster size threshold 100 voxels), post hoc Spearman's correlational analyses between food-evoked FDG signal change (FESC, FED minus FASTED) and ad libitum consumption at the FASTED visit were performed. Results: There were 10 clusters where the response to food ingestion was different between groups (previously reported). Correlations within each group between FESC in each cluster and ad libitum consumption are shown in the table. Mean+/-SD FESCs in cluster C were: NW -4.02 +/-2.48%, Ob -0.11+/-1.22%, RYGB -4.18+/-3.07%. Conclusion: The highly significant, strong, positive correlation in NW between FESC in cluster C (DLFC) and ad libitum consumption, with greater deactivation associated with lower ad libitum consumption, supports an association between DLFC deactivation (in this FDG-PET neuroimaging paradigm) and increased inhibitory control of food intake. There were no such correlations in Ob or RYGB. The mean FESCs in cluster C are consistent with low inhibitory control of food intake in the obese which is increased after RYGB and suggest altered DLFC activity after RYGB may contribute to weight loss. (figure present).&amp;nbsp;[Conference Abstract]&lt;/span&gt;

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