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Comparative Study
, 110-111, 122-8

Differences in the Neuronal Response to Food in Obesity-Resistant as Compared to Obesity-Prone Individuals

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Comparative Study

Differences in the Neuronal Response to Food in Obesity-Resistant as Compared to Obesity-Prone Individuals

Marc-Andre Cornier et al. Physiol Behav.

Abstract

Despite living in an obesogenic environment, some individuals maintain a thin phenotype compared to the majority who are at risk for weight gain and obesity. Understanding how these different phenotypes regulate energy intake is critical. The objective of this study was to examine the differences in neuronal response to visual food cues in adults recruited as either obesity-resistant (OR) or obesity-prone (OP) based on self-identification, BMI, and personal/family weight history. 25 OR and 28 OP individuals were studied after 4 days of eucaloric energy intake. Functional magnetic resonance imaging (fMRI) was performed in the fasted and acute fed states (30 min after a test meal) while subjects viewed images of foods of high hedonic value and neutral non-food objects. Measures of appetite using visual analog scales were performed before and every 30 min after the test meal for 3 h. In the fasted state, food as compared to nonfood images elicited significant response in the insula, somatosensory cortex, parietal cortex, and visual cortex in both OR and OP. The acute fed state resulted in significant attenuation of these and other brain areas in the OR but not OP individuals. Furthermore, OP as compared to OR individuals showed greater activation of medial and anterior prefrontal cortex (PFC) in response to the test meal. Adjusting for fat mass did not impact these results. Attenuation of insula/PFC response to food images in the fed state was associated with greater reductions in hunger. These findings suggest that individuals prone to weight gain and obesity have altered neuronal responses to food cues in brain regions known to be important in energy intake regulation. These altered responses may represent an important mechanism contributing to excess energy intake and risk for obesity.

Figures

Figure 1
Figure 1. Neuronal response to visual foods cues in obesity-resistant (OR) individuals in the fasted state
The neuronal response in OR individuals to visual stimuli of foods of high hedonic value as compared to non-food objects in the fasted state is shown. Robust activation is observed in the insula, sensory cortex, posterior cingulate, parietal cortex, and inferior temporal visual cortex. Statistical maps thresholded at a voxel-wise threshold of p < 0.01 and a cluster-level false discovery rate (FDR) threshold of q < 0.05 and overlaid onto the group averaged anatomical image. Data are shown in the neurological convention (right hemisphere on the right).
Figure 2
Figure 2. Neuronal response in fasted as compared to fed state in obesity-resistant (OR) individuals
The difference in neuronal response to foods of high hedonic value in the fasted as compared to fed state in OR individuals is shown. Reduced response in the insula and prefrontal cortex is observed after the test meal. Statistical maps thresholded at a voxel-wise threshold of p < 0.01 and a cluster-level false discovery rate (FDR) threshold of q < 0.05 and overlaid onto the group averaged anatomical image. Data are shown in the neurological convention (right hemisphere on the right).
Figure 3
Figure 3. Neuronal response in the fasted as compared to fed state in obesity-resistant (OR) as compared to obesity-prone (OP) individuals
The difference in neuronal response in the fasted as compared to fed state in OR as compared to OP individuals when viewing foods of high hedonic value is shown. Greater deactivation of the insula, prefrontal cortex (PFC) and medial PFC seen in OR as compared to OP individuals is shown in upper panel. Lower panel shows reductions in both insula/inferior PFC and medial prefrontal cortex in the fed as compared to fasted state in OR. In OP, the opposite effect was observed, with increased responses in these regions in the fed as compared to the fasted state. Statistical maps thresholded at a voxel-wise threshold of p < 0.01 and a cluster-level false discovery rate (FDR) threshold of q < 0.05 and overlaid onto the group averaged anatomical image. Data are shown in the neurological convention (right hemisphere on the right). Mean BOLD responses (± SEM) are shown for the insula/PFC and medial PFC.

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