Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Más filtros











Base de datos
Intervalo de año de publicación
1.
Endocrine ; 29(3): 391-8, 2006 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-16943575

RESUMEN

In the present study, we investigated the protein levels and phosphorylation status of the insulin receptor and insulin receptor substrates (IRS-1, IRS-2, and IRS-3) as well as their association with PI(3)-kinase in the rat adipose tissue of two models of insulin resistance: dexamethasone treatment and aging. AKT and atypical PKC phosphorylation detection were also performed. Both models showed decreased insulin-induced IRS-1 and IRS-2 tyrosine phosphorylation, accompanied by reduced protein levels of IRS-1 and IRS-2. Nevertheless, IRS-3 protein level was unchanged in aging but increased in dexamethasone-treated rats. PI(3)-kinase association with IRS-1 was reduced in aged rats, whereas dexamethasone-treated rats showed a reduced IRS-2/ PI(3)-kinase association. However, IRS-3 association with PI(3)-kinase was reduced in both models, as well as insulin-induced AKT and PKC phosphorylation. The alterations described in the present study show that the action of insulin is differently impaired depending on the origin of insulin resistance. These differences might be directly linked to the singular metabolic features of the models we tested.


Asunto(s)
Tejido Adiposo/metabolismo , Envejecimiento/fisiología , Dexametasona/farmacología , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Obesidad/metabolismo , Fosfoproteínas/metabolismo , Tejido Adiposo/efectos de los fármacos , Animales , Glucemia/análisis , Peso Corporal , Insulina/sangre , Proteínas Sustrato del Receptor de Insulina , Resistencia a la Insulina , Isoenzimas/metabolismo , Masculino , Fosfatidilinositol 3-Quinasas/metabolismo , Fosforilación , Proteína Quinasa C/metabolismo , Ratas , Ratas Wistar , Receptor de Insulina/metabolismo , Transducción de Señal/efectos de los fármacos
2.
J Endocrinol ; 190(2): 451-9, 2006 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-16899578

RESUMEN

Polycystic ovary syndrome (PCOS) manifests as chronic anovulation, ovarian hyperandrogenism, and follicular cysts, which are amplified by insulin as well as the inability of the hormone to stimulate glucose uptake in classic target tissues such as muscle and fat. In the present study, we evaluated the regulation of the insulin-signaling pathways by using immunoprecipitation and immunoblotting in whole extracts of ovaries from non-pregnant human chorionic gonadotropin (hCG)-treated rats, hyperinsulinemic-induced rats and hyperinsulinemic-induced rats, treated with hCG for 22 consecutive days. There were increased associations of insulin receptor substrate (IRS)-1 and IRS-2 with phosphatidylinositol (PI) 3-kinase, followed by enhanced protein kinase B (Akt) serine and threonine phosphorylation, in the ovaries of rats that were treated with hCG, either alone or with insulin. In contrast, the skeletal muscle demonstrated a reduced IRS-1/PI 3-kinase/Akt pathway in hyperinsulinemic-induced rats. These intracellular modifications were accompanied by follicular cysts, detected by optical microscopy, and increased androstenedione serum levels. In summary, our data show that chronic treatment with hCG or hCG plus insulin can induce changes in ovaries that simulate PCOS. In these situations, an increase in the insulin-induced IRS/PI 3-kinase/Akt pathway occurs in the ovary, suggesting that the activation of this pathway may have a role in the development of PCOS.


Asunto(s)
Gonadotropina Coriónica/farmacología , Insulina/farmacología , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal/efectos de los fármacos , Regulación hacia Arriba , Animales , Quinasas MAP Reguladas por Señal Extracelular/análisis , Femenino , Immunoblotting/métodos , Proteínas Sustrato del Receptor de Insulina , Péptidos y Proteínas de Señalización Intracelular/análisis , Proteína Oncogénica v-akt/análisis , Fosfoproteínas/análisis , Ratas , Ratas Wistar , Receptor de Insulina/análisis
3.
FEBS Lett ; 580(1): 285-90, 2006 Jan 09.
Artículo en Inglés | MEDLINE | ID: mdl-16376341

RESUMEN

The effect of dehydroepiandrosterone (DHEA) on pancreatic islet function of aged rats, an animal model with impaired glucose-induced insulin secretion, was investigated. The following parameters were examined: morphological analysis of endocrine pancreata by immunohistochemistry; protein levels of insulin receptor, IRS-1, IRS-2, PI 3-kinase, Akt-1, and Akt-2; and static insulin secretion in isolated pancreatic islets. Pancreatic islets from DHEA-treated rats showed an increased beta-cell mass accompanied by increased Akt-1 protein level but reduced IR, IRS-1, and IRS-2 protein levels and enhanced glucose-stimulated insulin secretion. The present results suggest that DHEA may be a promising drug to prevent diabetes during aging.


Asunto(s)
Adyuvantes Inmunológicos/administración & dosificación , Envejecimiento/metabolismo , Tamaño de la Célula/efectos de los fármacos , Deshidroepiandrosterona/administración & dosificación , Células Secretoras de Insulina/metabolismo , Insulina/metabolismo , Envejecimiento/efectos de los fármacos , Envejecimiento/patología , Animales , Diabetes Mellitus/tratamiento farmacológico , Diabetes Mellitus/metabolismo , Humanos , Inmunohistoquímica , Proteínas Sustrato del Receptor de Insulina , Secreción de Insulina , Células Secretoras de Insulina/patología , Péptidos y Proteínas de Señalización Intracelular , Masculino , Fosfatidilinositol 3-Quinasas/biosíntesis , Fosfoproteínas/biosíntesis , Proteínas Proto-Oncogénicas c-akt , Ratas , Ratas Wistar
4.
J Neurochem ; 90(3): 559-66, 2004 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-15255933

RESUMEN

Melatonin is the pineal hormone that acts via a pertussis toxin-sensitive G-protein to inhibit adenylate cyclase. However, the intracellular signalling effects of melatonin are not completely understood. Melatonin receptors are mainly present in the suprachiasmatic nucleus (SCN) and pars tuberalis of both humans and rats. The SCN directly controls, amongst other mechanisms, the circadian rhythm of plasma glucose concentration. In this study, using immunoprecipitation and immunoblotting, we show that melatonin induces rapid tyrosine phosphorylation and activation of the insulin receptor beta-subunit tyrosine kinase (IR) in the rat hypothalamic suprachiasmatic region. Upon IR activation, tyrosine phosphorylation of IRS-1 was detected. In addition, melatonin induced IRS-1/PI3-kinase and IRS-1/SHP-2 associations and downstream AKT serine phosphorylation and MAPK (mitogen-activated protein kinase) phosphorylation, respectively. These results not only indicate a new signal transduction pathway for melatonin, but also a potential cross-talk between melatonin and insulin.


Asunto(s)
Hipotálamo/efectos de los fármacos , Hipotálamo/metabolismo , Melatonina/farmacología , Proteínas Tirosina Quinasas/metabolismo , Animales , Relación Dosis-Respuesta a Droga , Inyecciones Intraventriculares , Insulina/farmacología , Proteínas Sustrato del Receptor de Insulina , Péptidos y Proteínas de Señalización Intracelular , Masculino , Proteína Quinasa 1 Activada por Mitógenos/efectos de los fármacos , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Fosfoproteínas/efectos de los fármacos , Fosfoproteínas/metabolismo , Fosforilación/efectos de los fármacos , Unión Proteica/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/metabolismo , Proteína Tirosina Fosfatasa no Receptora Tipo 11 , Proteínas Tirosina Fosfatasas/metabolismo , Proteínas Tirosina Quinasas/efectos de los fármacos , Proteínas Proto-Oncogénicas/efectos de los fármacos , Proteínas Proto-Oncogénicas/metabolismo , Proteínas Proto-Oncogénicas c-akt , Ratas , Ratas Wistar , Receptores de Melatonina/antagonistas & inhibidores , Receptores de Melatonina/metabolismo , Tetrahidronaftalenos/farmacología , Triptaminas/farmacología
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA