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Acta Physiol (Oxf) ; 228(2): e13345, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31310704

RESUMO

AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.


Assuntos
Ingestão de Alimentos/fisiologia , Hiperfagia/prevenção & controle , Região Hipotalâmica Lateral/efeitos dos fármacos , Leptina/farmacologia , Neurônios/metabolismo , Receptor Tipo 2 de Galanina/agonistas , Animais , Modelos Animais de Doenças , Ingestão de Alimentos/efeitos dos fármacos , Galanina/farmacologia , Grelina/metabolismo , Hiperfagia/metabolismo , Hiperfagia/patologia , Região Hipotalâmica Lateral/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Neurônios/efeitos dos fármacos , Orexinas/metabolismo , Receptor Tipo 2 de Galanina/metabolismo
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