Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
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Data(s) |
19/10/2012
19/10/2012
2009
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Resumo |
Uchoa ET, Sabino HA, Ruginsk SG, Antunes-Rodrigues J, Elias LL. Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses. J Appl Physiol 106: 596-604, 2009. First published November 20, 2008; doi: 10.1152/japplphysiol.90865.2008.-Glucocorticoids have major effects on food intake, demonstrated by the decrease of food intake following adrenalectomy. Satiety signals are relayed to the nucleus of the solitary tract (NTS), which has reciprocal projections with the arcuate nucleus (ARC) and paraventricular nucleus (PVN) of the hypothalamus. We evaluated the effects of glucocorticoids on the activation of hypothalamic and NTS neurons induced by food intake in rats subjected to adrenalectomy (ADX) or sham surgery 7 days before the experiments. One-half of ADX animals received corticosterone (ADX + B) in the drinking water (B: 25 mg/l). Fos/tyrosine hydroxylase (TH), Fos/corticotrophin-releasing factor (CRF) and Fos immunoreactivity were assessed in the NTS, PVN, and ARC, respectively. Food intake and body weight were reduced in the ADX group compared with sham and ADX + B groups. Fos and Fos/TH in the NTS, Fos, and Fos/CRF immunoreactive neurons in the PVN and Fos in the ARC were increased after refeeding, with higher number in the ADX group, compared with sham and ADX + B groups. CCK administration showed no hypophagic effect on ADX group despite a similar increase of Fos/TH immunoreactive neurons in the NTS compared with sham and ADX + B groups, suggesting that CCK alone cannot further increase the anorexigenic effect induced by glucocorticoid deficiency. The present data indicate that glucocorticoid withdrawal reduced food intake, which was associated with higher activation of ARC, CRF neurons of the PVN, and catecholaminergic neurons of the NTS. In the absence of glucocorticoids, satiety signals elicited during a meal lead to an augmented activation of brain stem and hypothalamic pathways. FAPESP Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, Brazil CAPES Coordenação de Aperfeiçoamento de Pessoal de Nível Superior CNPq Conselho Nacional de Desenvolvimento Cientifico e Tecnologico |
Identificador |
JOURNAL OF APPLIED PHYSIOLOGY, v.106, n.2, p.596-604, 2009 8750-7587 http://producao.usp.br/handle/BDPI/24423 10.1152/japplphysiol.90865.2008 |
Idioma(s) |
eng |
Publicador |
AMER PHYSIOLOGICAL SOC |
Relação |
Journal of Applied Physiology |
Direitos |
restrictedAccess Copyright AMER PHYSIOLOGICAL SOC |
Palavras-Chave | #glucocorticoids #food intake #satiety signals #nucleus of the solitary tract #paraventricular nucleus of the hypothalamus #arcuate nucleus of the hypothalamus #CORTICOTROPIN-RELEASING-FACTOR #DORSAL VAGAL COMPLEX #C-FOS EXPRESSION #NUCLEUS-TRACTUS-SOLITARIUS #DECREASES FOOD-INTAKE #RAT-BRAIN STEM #CATECHOLAMINERGIC NEURONS #PARAVENTRICULAR NUCLEUS #SPINAL-CORD #ENERGY HOMEOSTASIS #Physiology #Sport Sciences |
Tipo |
article original article publishedVersion |