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Review
. 2011 Sep 26;104(4):608-12.
doi: 10.1016/j.physbeh.2011.04.003. Epub 2011 Apr 9.

Is Your Brain to Blame for Weight Regain?

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Free PMC article
Review

Is Your Brain to Blame for Weight Regain?

Marc-Andre Cornier. Physiol Behav. .
Free PMC article

Abstract

Obesity is a serious and growing public health problem in the United States and the world. While weight loss is associated with significant benefits in obesity-related co-morbidities, successful long-term weight loss maintenance is extremely difficult. This limited success is primarily due to biologic mechanisms that clearly favor weight regain. The weight-reduced state is associated with not only reductions in energy expenditure and changes in substrate metabolism but also in increased energy intake. Measures of appetite (increased hunger, reduced satiety) clearly change with weight loss. These changes in appetite may be mediated by alterations of peripheral appetite-related signals, such as leptin and meal-related gut peptides, promoting energy intake. Furthermore, significant changes in the neuronal response to food-related cues in the weight-reduced state have also been shown, stressing the importance of the interactions between homeostatic and non-homeostatic regulation of energy intake. In summary, the weight-reduced state is clearly associated with a dysregulation of energy balance regulation, resulting in a milieu promoting weight regain, and thus being one of the major obstacles of "treating" obesity and reducing its comorbidities. This paper will review the adaptations in the central regulation of energy intake that occur after weight-loss or in the weight-reduce state in humans, including changes in peripheral appetite-related signals and neuroimaging studies examining the brain's response to weight loss.

Figures

Figure 1
Figure 1
The integration of homeostatic and non-homeostatic signals in the regulation of energy intake [15].
Figure 2
Figure 2
Mean (±SEM) pre-meal hunger (A) and post-meal satiety (B) during eucaloric and overfeeding diet periods are shown [18]. Overfeeding resulted in significant reductions in mean pre-meal hunger and increases in mean post-meal satiety in thin as compared to reduced-obese individuals.
Figure 3
Figure 3
The difference in neuronal response with overfeeding as compared to eucaloric feeding in reduced-obese as compared to thin individuals in response to foods of high hedonic value is shown [28]. A. Greater deactivation of the insula, hypothalamus and visual cortex is noted in thin as compared to reduced-obese individuals (p < 0.01). B. Mean BOLD responses (± SEM) are shown for the insula and hypothalamus.

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