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The Orexigenic Force of Olfactory Palatable Food Cues in Rats.

ABSTRACT: Environmental cues recalling palatable foods motivate eating beyond metabolic need, yet the timing of this response and whether it can develop towards a less palatable but readily available food remain elusive. Increasing evidence indicates that external stimuli in the olfactory modality communicate with the major hub in the feeding neurocircuitry, namely the hypothalamic arcuate nucleus (Arc), but the neural substrates involved have been only partially uncovered. By means of a home-cage hidden palatable food paradigm, aiming to mimic ubiquitous exposure to olfactory food cues in Western societies, we investigated whether the latter could drive the overeating of plain chow in non-food-deprived male rats and explored the neural mechanisms involved, including the possible engagement of the orexigenic ghrelin system. The olfactory detection of a familiar, palatable food impacted upon meal patterns, by increasing meal frequency, to cause the persistent overconsumption of chow. In line with the orexigenic response observed, sensing the palatable food in the environment stimulated food-seeking and risk-taking behavior, which are intrinsic components of food acquisition, and caused active ghrelin release. Our results suggest that olfactory food cues recruited intermingled populations of cells embedded within the feeding circuitry within the Arc, including, notably, those containing the ghrelin receptor. These data demonstrate the leverage of ubiquitous food cues, not only for palatable food searching, but also to powerfully drive food consumption in ways that resonate with heightened hunger, for which the orexigenic ghrelin system is implicated.

SUBMITTER: Peris-Sampedro F

PROVIDER: S-EPMC8471864 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Hypothalamic CRF1 receptor mechanisms are not sufficient to account for binge-like palatable food consumption in female rats.

Project description:OBJECTIVE:The present study evaluated the effect of systemic injection of the CRF1 receptor antagonist R121919, the corticosterone synthesis inhibitor metyrapone and central amygdala (CeA) injections of the nonselective CRF antagonist D-Phe-CRF(12-41) in rats in which binge eating was evoked by stress and cycles of food restriction. METHOD:Female rats were subjected or not to repeated cycles of regular chow food restriction/ad libitum feeding during which they were also given limited access (2 h) to palatable food. On the test day, rats were either exposed or not to the sight of the palatable food for 15 min without allowing access, before assessing food consumption. RESULTS:Systemic injections of R121919, but not of the metyrapone, blocked binge-like eating behavior. Restricted and stressed rats showed up-regulation of crh1 receptor mRNA signal in the bed nucleus of the stria terminalis and CeA but not in basolateral amygdala (BLA) or in the paraventricular nucleus. Injection D-Phe-CRF(12-41) in CeA but not in the BLA-blocked binge-like eating behavior. DISCUSSION:These findings demonstrate that extra-hypothalamic CRF1 receptors, rather than those involved in endocrine functions, are involved in binge eating and the crucial role of CRF receptors in CeA. CRF1 receptor antagonism may represent a novel pharmacological treatment for binge-related eating disorders.

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Nematophagous fungus Arthrobotrys oligospora mimics olfactory cues of sex and food to lure its nematode prey.

Project description:To study the molecular basis for predator-prey coevolution, we investigated how Caenorhabditis elegans responds to the predatory fungus Arthrobotrys oligospora. C. elegans and other nematodes were attracted to volatile compounds produced by A. oligospora. Gas-chromatographic mass-spectral analyses of A. oligospora-derived volatile metabolites identified several odors mimicking food cues attractive to nematodes. One compound, methyl 3-methyl-2-butenoate (MMB) additionally triggered strong sex- and stage-specific attraction in several Caenorhabditis species. Furthermore, when MMB is present, it interferes with nematode mating, suggesting that MMB might mimic sex pheromone in Caenorhabditis species. Forward genetic screening suggests that multiple receptors are involved in sensing MMB. Response to fungal odors involves the olfactory neuron AWCs. Single-cell RNA-seq revealed the GPCRs expressed in AWC. We propose that A. oligospora likely evolved the means to use olfactory mimicry to attract its nematode prey through the olfactory neurons in C. elegans and related species.

| S-EPMC5243009 | biostudies-literature

Discounting of Hyper-Palatable Food and Money: Associations with Food Addiction Symptoms.

Project description:IntroductionDelay discounting (DD), the tendency to prefer small, immediate rewards over larger, delayed rewards, is associated with health-risk behaviors. The study examined associations between DD for money and hyper-palatable foods (HPF) with food addiction (FA) symptoms among a general population sample.MethodsParticipants (N = 296) completed an adjusting DD task that consisted of a single-commodity condition with HPF as the reward (HPF now vs. HPF later) and cross-commodity conditions comparing money and HPF (money now vs. HPF later; HPF now vs. money later). The Yale Food Addiction Scale 2.0 was used to assess FA symptoms. Zero-inflated negative binomial regression models tested whether discounting of HPF and money was associated with FA symptoms.ResultsFindings indicated there were no significant associations between DD and FA symptoms in the single-commodity HPF condition (logit: OR = 1.02, p-value = 0.650; count: IRR = 1.04, p-value = 0.515). There were no significant associations among cross-commodity conditions comparing money now vs. HPF later (logit: OR = 0.96, p-value = 0.330; count: IRR = 1.02, p-value = 0.729) or conditions comparing HPF now vs. money later (logit: OR = 1.02, p-value = 0.682; count: IRR = 0.92, p-value = 0.128) and FA symptoms.ConclusionsDiscounting HPF may not be a key behavioral feature among individuals who endorse FA symptoms.

| S-EPMC10536694 | biostudies-literature

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