Document Detail

Is sprint exercise a leptin signaling mimetic in human skeletal muscle?
MedLine Citation:
PMID:  21659488     Owner:  NLM     Status:  MEDLINE    
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.
Borja Guerra; Hugo Olmedillas; Amelia Guadalupe-Grau; Jesús G Ponce-González; David Morales-Alamo; Teresa Fuentes; Esther Chapinal; Leandro Fernández-Pérez; Pedro De Pablos-Velasco; Alfredo Santana; Jose A L Calbet
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't     Date:  2011-06-09
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  111     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-09     Completed Date:  2012-01-11     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  715-25     Citation Subset:  IM    
Department of Physical Education, University of Las Palmas de Gran Canaria, Spain.
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MeSH Terms
Analysis of Variance
Blood Glucose / metabolism
Enzyme Activation
Fasting / metabolism
Gene Expression Regulation
Glucose / administration & dosage
Human Growth Hormone / blood
Interleukin-6 / blood
Janus Kinase 2 / metabolism
Leptin / blood,  metabolism*
Mitogen-Activated Protein Kinase 1 / metabolism
Mitogen-Activated Protein Kinase 3 / metabolism
Muscle Contraction* / genetics
Muscle, Skeletal / metabolism*
Protein Tyrosine Phosphatase, Non-Receptor Type 1 / metabolism
STAT3 Transcription Factor / metabolism
STAT5 Transcription Factor / metabolism
Signal Transduction* / genetics
Suppressor of Cytokine Signaling Proteins / metabolism
Time Factors
Young Adult
p38 Mitogen-Activated Protein Kinases / metabolism
Reg. No./Substance:
0/Blood Glucose; 0/IL6 protein, human; 0/Interleukin-6; 0/Leptin; 0/SOCS3 protein, human; 0/STAT3 Transcription Factor; 0/STAT3 protein, human; 0/STAT5 Transcription Factor; 0/Suppressor of Cytokine Signaling Proteins; 12629-01-5/Human Growth Hormone; 50-99-7/Glucose; EC protein, human; EC Kinase 2; EC protein, human; EC Protein Kinase 1; EC Protein Kinase 3; EC Mitogen-Activated Protein Kinases; EC protein, human; EC Tyrosine Phosphatase, Non-Receptor Type 1

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