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Corticotrophin-releasing factor mediates hypophagia after adrenalectomy, increasing meal-related satiety responses

Adrenalectomy-induced hypophagia is associated with increased satiety-related responses, which involve neuronal activation of the nucleus of the solitary tract (NTS). Besides its effects on the pituitary–adrenal axis, corticotrophin-releasing factor (CRF) has been shown to play an important role in...

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Published in:Hormones and behavior 2010-11, Vol.58 (5), p.714-719
Main Authors: Uchoa, Ernane Torres, da Silva, Lilian Eslaine Costa Mendes, de Castro, Margaret, Antunes-Rodrigues, Jose, Elias, Lucila Leico K.
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description Adrenalectomy-induced hypophagia is associated with increased satiety-related responses, which involve neuronal activation of the nucleus of the solitary tract (NTS). Besides its effects on the pituitary–adrenal axis, corticotrophin-releasing factor (CRF) has been shown to play an important role in feeding behaviour, as it possesses anorexigenic effects. We evaluated feeding-induced CRF mRNA expression in the paraventricular nucleus (PVN) and the effects of pretreatment with CRF 2 receptor antagonist (Antisauvagine-30, AS30) on food intake and activation of NTS neurons in response to feeding in adrenalectomised (ADX) rats. Compared to the sham group, ADX increased CRF mRNA levels in the PVN of fasted animals, which was further augmented by refeeding. AS30 treatment did not affect food intake in the sham and ADX + corticosterone (B) groups; however, it reversed hypophagia in the ADX group. In vehicle-pretreated animals, refeeding increased the number of Fos and Fos/TH-immunoreactive neurons in the NTS in the sham, ADX and ADX + B groups, with the highest number of neurons in the ADX animals. Similarly to its effect on food intake, pretreatment with AS30 in the ADX group also reversed the increased activation of NTS neurons induced by refeeding while having no effect in the sham and ADX + B animals. The present results show that adrenalectomy induces an increase in CRF mRNA expression in the PVN potentiated by feeding and that CRF 2 receptor antagonist abolishes the anorexigenic effect and the increased activation of NTS induced by feeding in the ADX animals. These data indicate that increased activity of PVN CRF neurons modulates brainstem satiety-related responses, contributing to hypophagia after adrenalectomy. ►Primary adrenal insufficiency increases meal-related satiety responses. ►Adrenalectomy-induced hypophagia is associated with increased CRF mRNA expression in the hypothalamic paraventricular nucleus (PVN) and increased NTS neuron activation in the brainstem. ►The increased activity of PVN CRF neurons modulates brainstem satiety-related responses. ►CRF type 2 receptor mediates CRF suppressing effect on food intake after adrenalectomy.
doi_str_mv 10.1016/j.yhbeh.2010.07.003
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Besides its effects on the pituitary–adrenal axis, corticotrophin-releasing factor (CRF) has been shown to play an important role in feeding behaviour, as it possesses anorexigenic effects. We evaluated feeding-induced CRF mRNA expression in the paraventricular nucleus (PVN) and the effects of pretreatment with CRF 2 receptor antagonist (Antisauvagine-30, AS30) on food intake and activation of NTS neurons in response to feeding in adrenalectomised (ADX) rats. Compared to the sham group, ADX increased CRF mRNA levels in the PVN of fasted animals, which was further augmented by refeeding. AS30 treatment did not affect food intake in the sham and ADX + corticosterone (B) groups; however, it reversed hypophagia in the ADX group. In vehicle-pretreated animals, refeeding increased the number of Fos and Fos/TH-immunoreactive neurons in the NTS in the sham, ADX and ADX + B groups, with the highest number of neurons in the ADX animals. Similarly to its effect on food intake, pretreatment with AS30 in the ADX group also reversed the increased activation of NTS neurons induced by refeeding while having no effect in the sham and ADX + B animals. The present results show that adrenalectomy induces an increase in CRF mRNA expression in the PVN potentiated by feeding and that CRF 2 receptor antagonist abolishes the anorexigenic effect and the increased activation of NTS induced by feeding in the ADX animals. These data indicate that increased activity of PVN CRF neurons modulates brainstem satiety-related responses, contributing to hypophagia after adrenalectomy. ►Primary adrenal insufficiency increases meal-related satiety responses. ►Adrenalectomy-induced hypophagia is associated with increased CRF mRNA expression in the hypothalamic paraventricular nucleus (PVN) and increased NTS neuron activation in the brainstem. ►The increased activity of PVN CRF neurons modulates brainstem satiety-related responses. ►CRF type 2 receptor mediates CRF suppressing effect on food intake after adrenalectomy.</description><identifier>ISSN: 0018-506X</identifier><identifier>EISSN: 1095-6867</identifier><identifier>DOI: 10.1016/j.yhbeh.2010.07.003</identifier><identifier>PMID: 20688066</identifier><identifier>CODEN: HOBEAO</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Adrenal glands ; Adrenalectomy - rehabilitation ; Animal behavior ; Animals ; Behavioral psychophysiology ; Biological and medical sciences ; Corticosterone - pharmacology ; Corticotrophin-releasing factor ; Corticotropin-Releasing Hormone - genetics ; Corticotropin-Releasing Hormone - metabolism ; Corticotropin-Releasing Hormone - physiology ; Down-Regulation - drug effects ; Eating - drug effects ; Eating - genetics ; Eating - physiology ; Feeding and Eating Disorders - chemically induced ; Feeding and Eating Disorders - genetics ; Feeding and Eating Disorders - metabolism ; Food ; Food intake ; Fundamental and applied biological sciences. 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Besides its effects on the pituitary–adrenal axis, corticotrophin-releasing factor (CRF) has been shown to play an important role in feeding behaviour, as it possesses anorexigenic effects. We evaluated feeding-induced CRF mRNA expression in the paraventricular nucleus (PVN) and the effects of pretreatment with CRF 2 receptor antagonist (Antisauvagine-30, AS30) on food intake and activation of NTS neurons in response to feeding in adrenalectomised (ADX) rats. Compared to the sham group, ADX increased CRF mRNA levels in the PVN of fasted animals, which was further augmented by refeeding. AS30 treatment did not affect food intake in the sham and ADX + corticosterone (B) groups; however, it reversed hypophagia in the ADX group. In vehicle-pretreated animals, refeeding increased the number of Fos and Fos/TH-immunoreactive neurons in the NTS in the sham, ADX and ADX + B groups, with the highest number of neurons in the ADX animals. Similarly to its effect on food intake, pretreatment with AS30 in the ADX group also reversed the increased activation of NTS neurons induced by refeeding while having no effect in the sham and ADX + B animals. The present results show that adrenalectomy induces an increase in CRF mRNA expression in the PVN potentiated by feeding and that CRF 2 receptor antagonist abolishes the anorexigenic effect and the increased activation of NTS induced by feeding in the ADX animals. 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Besides its effects on the pituitary–adrenal axis, corticotrophin-releasing factor (CRF) has been shown to play an important role in feeding behaviour, as it possesses anorexigenic effects. We evaluated feeding-induced CRF mRNA expression in the paraventricular nucleus (PVN) and the effects of pretreatment with CRF 2 receptor antagonist (Antisauvagine-30, AS30) on food intake and activation of NTS neurons in response to feeding in adrenalectomised (ADX) rats. Compared to the sham group, ADX increased CRF mRNA levels in the PVN of fasted animals, which was further augmented by refeeding. AS30 treatment did not affect food intake in the sham and ADX + corticosterone (B) groups; however, it reversed hypophagia in the ADX group. In vehicle-pretreated animals, refeeding increased the number of Fos and Fos/TH-immunoreactive neurons in the NTS in the sham, ADX and ADX + B groups, with the highest number of neurons in the ADX animals. Similarly to its effect on food intake, pretreatment with AS30 in the ADX group also reversed the increased activation of NTS neurons induced by refeeding while having no effect in the sham and ADX + B animals. The present results show that adrenalectomy induces an increase in CRF mRNA expression in the PVN potentiated by feeding and that CRF 2 receptor antagonist abolishes the anorexigenic effect and the increased activation of NTS induced by feeding in the ADX animals. These data indicate that increased activity of PVN CRF neurons modulates brainstem satiety-related responses, contributing to hypophagia after adrenalectomy. ►Primary adrenal insufficiency increases meal-related satiety responses. ►Adrenalectomy-induced hypophagia is associated with increased CRF mRNA expression in the hypothalamic paraventricular nucleus (PVN) and increased NTS neuron activation in the brainstem. ►The increased activity of PVN CRF neurons modulates brainstem satiety-related responses. ►CRF type 2 receptor mediates CRF suppressing effect on food intake after adrenalectomy.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>20688066</pmid><doi>10.1016/j.yhbeh.2010.07.003</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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subjects Adrenal glands
Adrenalectomy - rehabilitation
Animal behavior
Animals
Behavioral psychophysiology
Biological and medical sciences
Corticosterone - pharmacology
Corticotrophin-releasing factor
Corticotropin-Releasing Hormone - genetics
Corticotropin-Releasing Hormone - metabolism
Corticotropin-Releasing Hormone - physiology
Down-Regulation - drug effects
Eating - drug effects
Eating - genetics
Eating - physiology
Feeding and Eating Disorders - chemically induced
Feeding and Eating Disorders - genetics
Feeding and Eating Disorders - metabolism
Food
Food intake
Fundamental and applied biological sciences. Psychology
Gene Expression - drug effects
Glucocorticoids
Hormone Antagonists - pharmacology
Hormones
Hormones and behavior
Neurons
Neurons - drug effects
Neurons - metabolism
Nucleus of the solitary tract
Paraventricular Hypothalamic Nucleus - drug effects
Paraventricular Hypothalamic Nucleus - metabolism
Paraventricular nucleus of the hypothalamus
Peptide Fragments - pharmacology
Psychology. Psychoanalysis. Psychiatry
Psychology. Psychophysiology
Rats
Rats, Wistar
Receptors, Corticotropin-Releasing Hormone - antagonists & inhibitors
Rodents
Satiety Response - drug effects
Satiety Response - physiology
title Corticotrophin-releasing factor mediates hypophagia after adrenalectomy, increasing meal-related satiety responses
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