Hyperphagia and central mechanisms for leptin resistance during pregnancy (Registro nro. 6632)
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| 000 -CABECERA | |
|---|---|
| Campo de control de longitud fija | 03261na a2200229 4500 |
| 003 - IDENTIFICADOR DEL NÚMERO DE CONTROL | |
| Campo de control | H12O |
| 005 - FECHA Y HORA DE LA ÚLTIMA TRANSACCIÓN | |
| Campo de control | 20210625062804.0 |
| 008 - CÓDIGOS DE INFORMACIÓN DE LONGITUD FIJA | |
| Campo de control de longitud fija | 130622s2011 xxx||||| |||| 00| 0 eng d |
| 040 ## - FUENTE DE LA CATALOGACIÓN | |
| Centro transcriptor | H12O |
| 041 ## - CÓDIGO DE LENGUA | |
| Código de lengua del texto/banda sonora o título independiente | eng |
| 100 ## - PUNTO DE ACCESO PRINCIPAL - NOMBRE DE PERSONA | |
| Nombre de persona | Carro Díaz, Eva |
| 9 (RLIN) | 1777 |
| Término indicativo de función | Instituto de Investigación i+12 |
| 245 00 - MENCIÓN DE TÍTULO | |
| Título | Hyperphagia and central mechanisms for leptin resistance during pregnancy |
| Tipo de material | [artículo] |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. (IMPRINT) | |
| Nombre del editor distribuidor etc. | Endocrinology, |
| Fecha de publicación distribución etc. | 2011 |
| 300 ## - DESCRIPCIÓN FÍSICA | |
| Extensión | 152(4):1355-1365. |
| 500 ## - NOTA GENERAL | |
| Nota general | Formato Vancouver: Trujillo ML, Spuch C, Carro E, Señarís R. Hyperphagia and central mechanisms for leptin resistance during pregnancy. Endocrinology. 2011;152(4):1355-65. |
| 501 ## - NOTA DE “CON” | |
| Nota de "Con" | PMID: 21303957 |
| 504 ## - NOTA DE BIBLIOGRAFÍA; ETC. | |
| Nota de bibliografía etc. | Contiene 50 referencias |
| 520 ## - NOTA DE SUMARIO; ETC. | |
| Sumario etc. | The purpose of this work was to study the central mechanisms involved in food intake regulation and leptin resistance during gestation in the rat. Sprague Dawley rats of 7, 13, and 18 d of pregnancy [days of gestation (G) 7, G13, and G18] were used and compared with nonpregnant animals in diestrus-1. Food intake was already increased in G7, before hyperleptinemia and central leptin resistance was established in midpregnancy. Leptin resistance was due to a reduction in leptin transport through the blood-brain barrier (BBB) and to alterations in leptin signaling within the hypothalamus based on an increase in suppressor of cytokine signaling 3 levels and a blockade of signal transducer and activator of transcription-3 phosphorylation (G13), followed by a decrease in LepRb and of Akt phosphorylation (G18). In early gestation (G7), no change in hypothalamic neuropeptide Y (NPY), agouti-related peptide (AgRP), or proopiomelanocortin (POMC) expression was shown. Nevertheless, an increase in NPY and AgRP and a decrease in POMC mRNA were observed in G13 and G18 rats, probably reflecting the leptin resistance. To investigate the effect of maternal vs. placental hormones on these mechanisms, we used a model of pseudogestation. Rats of 9 d of pseudogestation were hyperphagic, showing an increase in body and adipose tissue weight, normoleptinemia, and normal responses to iv/intracerebroventricular leptin on hypothalamic leptin signaling, food intake, and body weight. Leptin transport through the BBB, and hypothalamic NPY, AgRP and POMC expression were unchanged. Finally, the transport of leptin through the BBB was assessed using a double-chamber culture system of choroid plexus epithelial cells or brain microvascular endothelial cells. We found that sustained high levels of prolactin significantly reduced leptin translocation through the barrier, whereas progesterone and β-estradiol did not show any effect. Our data demonstrate a dual mechanism of leptin resistance during mid/late-pregnancy, which is not due to maternal hormones and which allows the maintenance of hyperphagia in the presence of hyperleptinemia driven by an increase in NPY and AgRP and a decrease in POMC mRNA. By contrast, in early pregnancy maternal hormones induce hyperphagia without the regulation of hypothalamic NPY, AgRP, or POMC and in the absence of leptin resistance. |
| 710 ## - PUNTO DE ACCESO ADICIONAL - NOMBRE DE ENTIDAD | |
| 9 (RLIN) | 625 |
| Nombre de entidad o nombre de jurisdicción como elemento inicial | Instituto de Investigación imas12 |
| 856 ## - LOCALIZACIÓN Y ACCESO ELECTRÓNICOS | |
| Identificador Uniforme del Recurso (URI) | http://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/6/pc6632.pdf |
| Acceso | Solicitar documento |
| 942 ## - ENTRADA PARA ELEMENTOS AGREGADOS (KOHA) | |
| Suprimido en OPAC | Público |
| Fuente de clasificación o esquema de ordenación en estanterías | |
| Koha [por defecto] tipo de item | Artículo |
| Suprimido | Estado de pérdida | Fuente de clasificación o esquema de ordenación en estanterías | Estropeado | No para préstamo | Localización permanente | Localización actual | Fecha de adquisición | Signatura completa | Fecha última consulta | Fecha del precio de reemplazo | Tipo de item de Koha |
|---|---|---|---|---|---|---|---|---|---|---|---|
| Hospital Universitario 12 de Octubre | Hospital Universitario 12 de Octubre | 2016-01-29 | PC6632 | 2016-01-29 | 2016-01-29 | Artículo |
