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1.
J Neural Transm (Vienna) ; 117(9): 1077-81, 2010 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-20690033

RESUMEN

Genes involved in alcoholism have consensus sites for the transcription factor activator protein (TFAP) 2beta. In the present study, we investigated TFAP-2beta protein levels in the ethanol-preferring alko, alcohol (AA) and the ethanol-avoiding alko, non-alcohol (ANA) rat lines. Furthermore, basal and ethanol-induced TFAP-2beta levels were examined in Wistar rats exposed to different early postnatal environments that are known to affect later ethanol consumption. Taken together, we found differences in brainstem TFAP-2beta protein between the AA and ANA rats.


Asunto(s)
Consumo de Bebidas Alcohólicas/metabolismo , Tronco Encefálico/metabolismo , Etanol/farmacología , Privación Materna , Medio Social , Factor de Transcripción AP-2/metabolismo , Consumo de Bebidas Alcohólicas/genética , Análisis de Varianza , Animales , Ratas , Ratas Wistar , Factor de Transcripción AP-2/genética
2.
J Neuroendocrinol ; 21(9): 777-85, 2009 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-19703102

RESUMEN

In the present study, we explore the central nervous system mechanism underlying the chronic central effects of ghrelin with respect to increasing body weight and body fat. Specifically, using a recently developed ghrelin receptor antagonist, GHS-R1A (JMV2959), we investigate the role of GHS-R1A in mediating the effects of ghrelin on energy balance and on hypothalamic gene expression. As expected, in adult male rats, chronic central treatment with ghrelin for 14 days, when compared to vehicle-treated control rats, resulted in an increased body weight, lean mass and fat mass (assessed by dual X-ray absorptiometry), dissected white fat pad weight, cumulative food intake, food efficiency, respiratory exchange ratio and a decrease of energy expenditure. Co-administration of the ghrelin receptor antagonist JMV2959 suppressed/blocked the majority of these effects, with the notable exception of ghrelin-induced food intake and food efficiency. The hypothesis emerging from these data, namely that GHS-R1A mediates the chronic effects of ghrelin on fat accumulation, at least partly independent of food intake, is discussed in light of the accompanying data regarding the hypothalamic genes coding for peptides and receptors involved in energy balance regulation, which were found to have altered expression in these studies.


Asunto(s)
Sistema Nervioso Central/efectos de los fármacos , Ghrelina/farmacología , Antagonistas de Hormonas/farmacología , Obesidad/inducido químicamente , Receptores de Ghrelina/antagonistas & inhibidores , Animales , Composición Corporal/efectos de los fármacos , Peso Corporal/efectos de los fármacos , Sistema Nervioso Central/metabolismo , Sistema Nervioso Central/fisiología , Ingestión de Alimentos/efectos de los fármacos , Expresión Génica/efectos de los fármacos , Ghrelina/administración & dosificación , Ghrelina/efectos adversos , Ghrelina/antagonistas & inhibidores , Hormonas/sangre , Hipotálamo/efectos de los fármacos , Hipotálamo/metabolismo , Inyecciones Intraventriculares , Masculino , Obesidad/sangre , Ratas , Ratas Sprague-Dawley , Transducción de Señal/efectos de los fármacos
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