Neuroendocrine Modulation of Food Intake and Eating Behavior.
Eating behavior
cholecystokinin
food intake
ghrelin
glucagon-like-peptide-1
leptin
nesfatin-1
neuroendocrine modulation
oxytocin
peptide YY
Journal
Endocrine, metabolic & immune disorders drug targets
ISSN: 2212-3873
Titre abrégé: Endocr Metab Immune Disord Drug Targets
Pays: United Arab Emirates
ID NLM: 101269157
Informations de publication
Date de publication:
2022
2022
Historique:
received:
12
05
2021
revised:
06
11
2021
accepted:
24
12
2021
pubmed:
29
1
2022
medline:
3
12
2022
entrez:
28
1
2022
Statut:
ppublish
Résumé
In the first section of this review, we examined the neuroanatomical and neurochemical data on hunger and satiety centers, glucose receptors, sensorial influences on eating behavior, and regulation of energy requirements. The second section is devoted to orexigenic and anorexigenic hormones. This paper aimed to overview and summarize data regarding the role of neuroendocrine regulation of food intake and eating behavior. Appropriate keywords and MeSH terms were identified and searched in MEDLINE/ PubMed. References of original articles and reviews were examined. Hunger and satiety center are located in the lateral (LH) and ventromedial hypothalamus (VMH). Lasting aphagia has been observed following a lesion of LH, while hyperphagia is induced by LH stimulation. On the other hand, increased food intake after VMH lesion and aphagia following VMH stimulation in hungry animals has also been reported. Intracellular glucopenia triggers food intake by reducing neuronal activity at the satiety center level. Moreover, sensory influences are regulated by food palatability as the positive hedonic evaluation of food and energy requirement indicates the average amount of food energy needed to balance energy expenditure. Orexigenic and anorexigenic hormones secreted from the gastrointestinal tract and adipose tissue regulate brain areas involved in eating behavior via gastric afferent vagal nerve, circumventricular organ area postrema, or transporter system. Finally, oxytocin (OT) plays a role in reward-related eating by inhibiting sugar intake and decreasing palatable food intake by suppressing the reward circuitry in the brain. Moreover, the anorectic effect of nesfatin-1 is abolished by an OT antagonist.
Sections du résumé
BACKGROUND
BACKGROUND
In the first section of this review, we examined the neuroanatomical and neurochemical data on hunger and satiety centers, glucose receptors, sensorial influences on eating behavior, and regulation of energy requirements. The second section is devoted to orexigenic and anorexigenic hormones.
OBJECTIVE
OBJECTIVE
This paper aimed to overview and summarize data regarding the role of neuroendocrine regulation of food intake and eating behavior.
METHODS
METHODS
Appropriate keywords and MeSH terms were identified and searched in MEDLINE/ PubMed. References of original articles and reviews were examined.
RESULTS
RESULTS
Hunger and satiety center are located in the lateral (LH) and ventromedial hypothalamus (VMH). Lasting aphagia has been observed following a lesion of LH, while hyperphagia is induced by LH stimulation. On the other hand, increased food intake after VMH lesion and aphagia following VMH stimulation in hungry animals has also been reported. Intracellular glucopenia triggers food intake by reducing neuronal activity at the satiety center level. Moreover, sensory influences are regulated by food palatability as the positive hedonic evaluation of food and energy requirement indicates the average amount of food energy needed to balance energy expenditure. Orexigenic and anorexigenic hormones secreted from the gastrointestinal tract and adipose tissue regulate brain areas involved in eating behavior via gastric afferent vagal nerve, circumventricular organ area postrema, or transporter system. Finally, oxytocin (OT) plays a role in reward-related eating by inhibiting sugar intake and decreasing palatable food intake by suppressing the reward circuitry in the brain. Moreover, the anorectic effect of nesfatin-1 is abolished by an OT antagonist.
Identifiants
pubmed: 35086464
pii: EMIDDT-EPUB-120457
doi: 10.2174/1871530322666220127114326
doi:
Substances chimiques
Oxytocin
50-56-6
Types de publication
Review
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1252-1262Informations de copyright
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