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Neural circuits for cognitive appetite control in healthy and obese individuals: an fMRI study.

Tuulari JJ, Karlsson HK, Hirvonen J, Salminen P, Nuutila P, Nummenmaa L - PLoS ONE (2015)

Bottom Line: They were instructed to inhibit their urge to eat the foods, view the stimuli passively or imagine eating the foods.Inhibition minus imagined eating (appetite control) activated bilateral precunei and parietal cortices and frontal regions spanning anterior cingulate and superior medial frontal cortices.During appetite control, obese subjects had lower responses in the medial frontal, middle cingulate and dorsal caudate nuclei.

View Article: PubMed Central - PubMed

Affiliation: Turku PET Centre, University of Turku, Turku, Finland.

ABSTRACT
The mere sight of foods may activate the brain's reward circuitry, and humans often experience difficulties in inhibiting urges to eat upon encountering visual food signals. Imbalance between the reward circuit and those supporting inhibitory control may underlie obesity, yet brain circuits supporting volitional control of appetite and their possible dysfunction that can lead to obesity remain poorly specified. Here we delineated the brain basis of volitional appetite control in healthy and obese individuals with functional magnetic resonance imaging (fMRI). Twenty-seven morbidly obese women (mean BMI = 41.4) and fourteen age-matched normal-weight women (mean BMI = 22.6) were scanned with 1.5 Tesla fMRI while viewing food pictures. They were instructed to inhibit their urge to eat the foods, view the stimuli passively or imagine eating the foods. Across all subjects, a frontal cortical control circuit was activated during appetite inhibition versus passive viewing of the foods. Inhibition minus imagined eating (appetite control) activated bilateral precunei and parietal cortices and frontal regions spanning anterior cingulate and superior medial frontal cortices. During appetite control, obese subjects had lower responses in the medial frontal, middle cingulate and dorsal caudate nuclei. Functional connectivity of the control circuit was increased in morbidly obese versus control subjects during appetite control, which might reflect impaired integrative and executive function in obesity.

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Regional differences in brain activations between normal-weight and obese subjects.Brain regions showing stronger activation in normal-weight versus morbidly obese subjects in inhibition minus passive viewing (A), imaginary eating minus passive viewing (B) and inhibition minus versus imaginary eating (C) contrasts. The data in C are thresholded at p < 0.05, FDR corrected at cluster level (p < 0.005, uncorrected at A and B).
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pone.0116640.g003: Regional differences in brain activations between normal-weight and obese subjects.Brain regions showing stronger activation in normal-weight versus morbidly obese subjects in inhibition minus passive viewing (A), imaginary eating minus passive viewing (B) and inhibition minus versus imaginary eating (C) contrasts. The data in C are thresholded at p < 0.05, FDR corrected at cluster level (p < 0.005, uncorrected at A and B).

Mentions: In inhibition minus imaginary eating comparison, normal-weight subjects showed stronger activations than obese subjects in bilateral dorsal caudate nuclei and anterior cingulate cortex (Fig. 3C, Table 5). Correspondingly, obese subjects had greater activations in the bilateral posterior cingulum (Table 5). Other contrasts of interest revealed no significant activations at our a priori statistical threshold. Using a slightly more lenient statistical threshold (p < 0.005, uncorrected as compared to a priori threshold of p < 0.05, FDR corrected), we found that in inhibition vs. passive viewing comparison, normal-weight subjects had stronger responses in the left middle and inferior frontal gyri, and right orbitofrontal cortex (OFC), and obese subjects had greater activation of bilateral posterior cingulum (Fig. 3A, Table 5). When contrasting imaginary eating minus passive viewing, healthy subjects showed stronger right-hemispheric insular activation (Fig. 3B, Table 5).


Neural circuits for cognitive appetite control in healthy and obese individuals: an fMRI study.

Tuulari JJ, Karlsson HK, Hirvonen J, Salminen P, Nuutila P, Nummenmaa L - PLoS ONE (2015)

Regional differences in brain activations between normal-weight and obese subjects.Brain regions showing stronger activation in normal-weight versus morbidly obese subjects in inhibition minus passive viewing (A), imaginary eating minus passive viewing (B) and inhibition minus versus imaginary eating (C) contrasts. The data in C are thresholded at p < 0.05, FDR corrected at cluster level (p < 0.005, uncorrected at A and B).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4320085&req=5

pone.0116640.g003: Regional differences in brain activations between normal-weight and obese subjects.Brain regions showing stronger activation in normal-weight versus morbidly obese subjects in inhibition minus passive viewing (A), imaginary eating minus passive viewing (B) and inhibition minus versus imaginary eating (C) contrasts. The data in C are thresholded at p < 0.05, FDR corrected at cluster level (p < 0.005, uncorrected at A and B).
Mentions: In inhibition minus imaginary eating comparison, normal-weight subjects showed stronger activations than obese subjects in bilateral dorsal caudate nuclei and anterior cingulate cortex (Fig. 3C, Table 5). Correspondingly, obese subjects had greater activations in the bilateral posterior cingulum (Table 5). Other contrasts of interest revealed no significant activations at our a priori statistical threshold. Using a slightly more lenient statistical threshold (p < 0.005, uncorrected as compared to a priori threshold of p < 0.05, FDR corrected), we found that in inhibition vs. passive viewing comparison, normal-weight subjects had stronger responses in the left middle and inferior frontal gyri, and right orbitofrontal cortex (OFC), and obese subjects had greater activation of bilateral posterior cingulum (Fig. 3A, Table 5). When contrasting imaginary eating minus passive viewing, healthy subjects showed stronger right-hemispheric insular activation (Fig. 3B, Table 5).

Bottom Line: They were instructed to inhibit their urge to eat the foods, view the stimuli passively or imagine eating the foods.Inhibition minus imagined eating (appetite control) activated bilateral precunei and parietal cortices and frontal regions spanning anterior cingulate and superior medial frontal cortices.During appetite control, obese subjects had lower responses in the medial frontal, middle cingulate and dorsal caudate nuclei.

View Article: PubMed Central - PubMed

Affiliation: Turku PET Centre, University of Turku, Turku, Finland.

ABSTRACT
The mere sight of foods may activate the brain's reward circuitry, and humans often experience difficulties in inhibiting urges to eat upon encountering visual food signals. Imbalance between the reward circuit and those supporting inhibitory control may underlie obesity, yet brain circuits supporting volitional control of appetite and their possible dysfunction that can lead to obesity remain poorly specified. Here we delineated the brain basis of volitional appetite control in healthy and obese individuals with functional magnetic resonance imaging (fMRI). Twenty-seven morbidly obese women (mean BMI = 41.4) and fourteen age-matched normal-weight women (mean BMI = 22.6) were scanned with 1.5 Tesla fMRI while viewing food pictures. They were instructed to inhibit their urge to eat the foods, view the stimuli passively or imagine eating the foods. Across all subjects, a frontal cortical control circuit was activated during appetite inhibition versus passive viewing of the foods. Inhibition minus imagined eating (appetite control) activated bilateral precunei and parietal cortices and frontal regions spanning anterior cingulate and superior medial frontal cortices. During appetite control, obese subjects had lower responses in the medial frontal, middle cingulate and dorsal caudate nuclei. Functional connectivity of the control circuit was increased in morbidly obese versus control subjects during appetite control, which might reflect impaired integrative and executive function in obesity.

Show MeSH
Related in: MedlinePlus