Abstract

Non-homeostatic hyperphagia, which is a major contributor to obesity-related hyperalimentation, is associated with the diet’s molecular composition influencing, for example, the energy content. Thus, specific food items such as snack food may induce food intake independent from the state of satiety. To elucidate mechanisms how snack food may induce non-homeostatic food intake, it was tested if manganese-enhanced magnetic resonance imaging (MEMRI) was suitable for mapping the whole brain activity related to standard and snack food intake under normal behavioral situation. Application of the MnCl2 solution by osmotic pumps ensured that food intake was not significantly affected by the treatment. After z-score normalization and a non-affine three-dimensional registration to a rat brain atlas, significantly different grey values of 80 predefined brain structures were recorded in ad libitum fed rats after the intake of potato chips compared to standard chow at the group level. Ten of these areas had previously been connected to food intake, in particular to hyperphagia (e.g. dorsomedial hypothalamus or the anterior paraventricular thalamic nucleus) or to the satiety system (e.g. arcuate hypothalamic nucleus or solitary tract); 27 areas were related to reward/addiction including the core and shell of the nucleus accumbens, the ventral pallidum and the ventral striatum (caudate and putamen). Eleven areas associated to sleep displayed significantly reduced Mn2+-accumulation and six areas related to locomotor activity showed significantly increased Mn2+-accumulation after the intake of potato chips. The latter changes were associated with an observed significantly higher locomotor activity. Osmotic pump-assisted MEMRI proved to be a promising technique for functional mapping of whole brain activity patterns associated to nutritional intake under normal behavior.

Highlights

  • Hyperphagia, which is associated with caloric hyperalimentation, substantially contributes to the development of obesity and obesity-related complications in industrial societies [1]

  • Whereas homeostatic hyperphagia is caused by a disturbance of the homeostatic system that regulates hunger and satiety, hedonic hyperphagia is rather independent from satiety [1]

  • The present study investigated specific brain activity patterns related to the intake of snack food compared to standard chow

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Summary

Introduction

Hyperphagia, which is associated with caloric hyperalimentation, substantially contributes to the development of obesity and obesity-related complications in industrial societies [1]. Whereas homeostatic hyperphagia is caused by a disturbance of the homeostatic system that regulates hunger and satiety, hedonic hyperphagia is rather independent from satiety [1]. The mechanisms, that override the physiological regulation of hunger and food intake are not fully elucidated. Food intake may activate the brain reward system in a way that overcompensates the homeostatic control of appetite [2]. The resulting hedonic hyperphagia is influenced by several factors such as the consumer’s emotional state, mental health conditions or sleep deprivation [1]. It is well documented that ‘‘palatable food’’ may induce hyperphagia in humans and animals [3,4]. Binge eating episodes in humans, for example, often involve food rich in fats or sugars, or both [5]

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