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Food cue reactivity: Neurobiological and behavioral underpinnings

The modern obesogenic environment contains an abundance of food cues (e.g., sight, smell of food) as well cues that are associated with food through learning and memory processes. Food cue exposure can lead to food seeking and excessive consumption in otherwise food-sated individuals, and a high lev...

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Autores principales: Kanoski, Scott E., Boutelle, Kerri N.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9307541/
https://www.ncbi.nlm.nih.gov/pubmed/35482137
http://dx.doi.org/10.1007/s11154-022-09724-x
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author Kanoski, Scott E.
Boutelle, Kerri N.
author_facet Kanoski, Scott E.
Boutelle, Kerri N.
author_sort Kanoski, Scott E.
collection PubMed
description The modern obesogenic environment contains an abundance of food cues (e.g., sight, smell of food) as well cues that are associated with food through learning and memory processes. Food cue exposure can lead to food seeking and excessive consumption in otherwise food-sated individuals, and a high level of food cue responsivity is a risk factor for overweight and obesity. Similar food cue responses are observed in experimental rodent models, and these models are therefore useful for mechanistically identifying the neural circuits mediating food cue responsivity. This review draws from both experimental rodent models and human data to characterize the behavioral and biological processes through which food-associated stimuli contribute to overeating and weight gain. Two rodent models are emphasized – cue-potentiated feeding and Pavlovian-instrumental transfer – that provide insight in the neural circuits and peptide systems underlying food cue responsivity. Data from humans are highlighted that reveal physiological, psychological, and neural mechanisms that connect food cue responsivity with overeating and weight gain. The collective literature identifies connections between heightened food cue responsivity and obesity in both rodents and humans, and identifies underlying brain regions (nucleus accumbens, amygdala, orbitofrontal cortex, hippocampus) and endocrine systems (ghrelin) that regulate food cue responsivity in both species. These species similarities are encouraging for the possibility of mechanistic rodent model research and further human research leading to novel treatments for excessive food cue responsivity in humans.
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spelling pubmed-93075412022-07-24 Food cue reactivity: Neurobiological and behavioral underpinnings Kanoski, Scott E. Boutelle, Kerri N. Rev Endocr Metab Disord Article The modern obesogenic environment contains an abundance of food cues (e.g., sight, smell of food) as well cues that are associated with food through learning and memory processes. Food cue exposure can lead to food seeking and excessive consumption in otherwise food-sated individuals, and a high level of food cue responsivity is a risk factor for overweight and obesity. Similar food cue responses are observed in experimental rodent models, and these models are therefore useful for mechanistically identifying the neural circuits mediating food cue responsivity. This review draws from both experimental rodent models and human data to characterize the behavioral and biological processes through which food-associated stimuli contribute to overeating and weight gain. Two rodent models are emphasized – cue-potentiated feeding and Pavlovian-instrumental transfer – that provide insight in the neural circuits and peptide systems underlying food cue responsivity. Data from humans are highlighted that reveal physiological, psychological, and neural mechanisms that connect food cue responsivity with overeating and weight gain. The collective literature identifies connections between heightened food cue responsivity and obesity in both rodents and humans, and identifies underlying brain regions (nucleus accumbens, amygdala, orbitofrontal cortex, hippocampus) and endocrine systems (ghrelin) that regulate food cue responsivity in both species. These species similarities are encouraging for the possibility of mechanistic rodent model research and further human research leading to novel treatments for excessive food cue responsivity in humans. Springer US 2022-04-28 2022 /pmc/articles/PMC9307541/ /pubmed/35482137 http://dx.doi.org/10.1007/s11154-022-09724-x Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. (https://creativecommons.org/licenses/by/4.0/)
spellingShingle Article
Kanoski, Scott E.
Boutelle, Kerri N.
Food cue reactivity: Neurobiological and behavioral underpinnings
title Food cue reactivity: Neurobiological and behavioral underpinnings
title_full Food cue reactivity: Neurobiological and behavioral underpinnings
title_fullStr Food cue reactivity: Neurobiological and behavioral underpinnings
title_full_unstemmed Food cue reactivity: Neurobiological and behavioral underpinnings
title_short Food cue reactivity: Neurobiological and behavioral underpinnings
title_sort food cue reactivity: neurobiological and behavioral underpinnings
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9307541/
https://www.ncbi.nlm.nih.gov/pubmed/35482137
http://dx.doi.org/10.1007/s11154-022-09724-x
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