Abstract

Since foods with high hedonic value are often consumed in excess of energetic needs, this study was designed to identify the mechanisms that may counter anorexigenic signalling in the presence of hedonic foods in lean animals. Mice, in different states of satiety (fed/fasted, or fed/fasted and treated with ghrelin or leptin, respectively), were allowed to choose between high-fat/high-sucrose and standard foods. Intake of each food type and the activity of hypothalamic neuropetidergic neurons that regulate appetite were monitored. In some cases, food choice was monitored in leptin-injected fasted mice that received microinjections of galanin receptor agonists into the lateral hypothalamus. Appetite-stimulating orexin neurons in the lateral hypothalamus are rapidly activated when lean, satiated mice consume a highly palatable food (PF); such activation (upregulated c-Fos expression) occurred even after administration of the anorexigenic hormone leptin and despite intact leptin signalling in the hypothalamus. The ability of leptin to restrain PF eating is restored when a galanin receptor 2 (Gal2R) agonist is injected into the lateral hypothalamus. Hedonically-loaded foods interrupt the inhibitory actions of leptin on orexin neurons and interfere with the homeostatic control of feeding. Overeating of palatable foods can be curtailed in lean animals by activating Gal2R in the lateral hypothalamus.

Highlights

  • The abundance and convenience of energy‐rich foods with high hedonic value poses a homeostatic challenge for modern humans and predisposes them to obesity and associated cardiometabolic and psychiatric diseases.[1]

  • Brain areas possibly contributing to hedonic eating were mapped using immediate early gene c‐Fos, and c‐Fos was monitored in first‐ and second‐order neurons (POMC, OX); in addition, we examined the efficacy of leptin signalling[11,12] when leptin‐treated mice were confronted with hedonically‐loaded palatable food (PF)

  • We here examined the hypothesis that disruption of the homeostatic processes that normally signal satiety and terminate eating are disrupted upon initial encounters with palatable foods that have high hedonic value, resulting in their overconsumption.[5]

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Summary

| INTRODUCTION

The abundance and convenience of energy‐rich foods with high hedonic value poses a homeostatic challenge for modern humans and predisposes them to obesity and associated cardiometabolic and psychiatric diseases.[1] While the maladaptive peripheral and central responses to chronic overeating have been extensively explored,[2,3,4] present knowledge of the. These observations suggest that descending hedonic information impinges on Gal neurons which, in turn, gate the access of peripheral signals of satiety to OX neurons

| RESULTS
| DISCUSSION
| MATERIALS AND METHODS
Findings
CONFLICT OF INTEREST

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