Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/44481
Título: Is sprint exercise a leptin signaling mimetic in human skeletal muscle?
Autores/as: Guerra, Borja 
Olmedillas, Hugo
Guadalupe Grau, Amelia 
Ponce-González, Jesús G.
Morales Alamo, David 
Fuentes, Teresa
Chapinal, Esther 
Fernández-Pérez, Leandro 
De Pablos Velasco, Pedro Luis 
Santana Rodríguez, Alfredo 
Calbet, Jose A. L. 
Clasificación UNESCO: 241106 Fisiología del ejercicio
Palabras clave: IL-6
SOCS3
STAT3
p38 MAPK
Fecha de publicación: 2011
Proyectos: Influencia Del Polimorfismo Del Gen Del Receptor de la Vitamina D y Del Fenotipo Muscular en la Respuesta Osteogénica Al Ejercicio Con y Sin Impactos en Seres Humanos. 
Influencia Del Ejercicio Físico en Los Mecanismos de Señalización de Leptina en El Músculo Esquelético Humano. 
Mecanismos Fisiológicos y Moleculares de la Reducción de Masa Grasa en Seres Humanos Mediante Ejercicios de Musculación. 
Integracion de Los Grupos de la Obesidad y El Síndrome Metabólico .... 
Publicación seriada: Journal of Applied Physiology 
Resumen: This study was designed to determine whether sprint exercise activates signaling cascades linked to leptin actions in human skeletal muscle and how this pattern of activation may be interfered by glucose ingestion. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before the Wingate test. Exercise elicited different patterns of JAK2, STAT3, STAT5, ERK1/2, p38 MAPK phosphorylation, and SOCS3 protein expression during the recovery period after glucose ingestion. Thirty minutes after the control sprint, STAT3 and ERK1/2 phosphorylation levels were augmented (both, P < 0.05). SOCS3 protein expression was increased 120 min after the control sprint but PTP1B protein expression was unaffected. Thirty and 120 min after the control sprint, STAT5 phosphorylation was augmented (P < 0.05). Glucose abolished the 30 min STAT3 and ERK1/2 phosphorylation and the 120 min SOCS3 protein expression increase while retarding the STAT5 phosphorylation response to sprint. Activation of these signaling cascades occurred despite a reduction of circulating leptin concentration after the sprint. Basal JAK2 and p38 MAPK phosphorylation levels were reduced and increased (both P < 0.05), respectively, by glucose ingestion prior to exercise. During recovery, JAK2 phosphorylation was unchanged and p38 MAPK phosphorylation was transiently reduced when the exercise was preceded by glucose ingestion. In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.
URI: http://hdl.handle.net/10553/44481
ISSN: 8750-7587
DOI: 10.1152/japplphysiol.00805.2010
Fuente: Journal Of Applied Physiology [ISSN 8750-7587],v. 111 (3), p. 715-725, (Septiembre 2011)
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