Document Detail

MedLine Citation:
PMID:  21212094     Owner:  NLM     Status:  Publisher    
Endurance exercise is known to enhance peripheral insulin sensitivity and reduce insulin secretion. However, it is unknown if the latter effect is due to the reduction in plasma substrate availability or alterations in β -cells secretory machinery. Here, we tested the hypothesis that endurance exercise reduces insulin secretion by altering the intracellular energy sensitive AMP-activated kinase (AMPK) signaling pathway. Male Wistar rats were submitted to endurance protocol training, one, three or five times per week, during eight weeks. After that, pancreatic islets were isolated and glucose-induced insulin secretion (GIIS), glucose transporter 2 (GLUT2) protein content, total and phophorylated calmodulin kinase kinase (CaMKII), and AMPK levels as well as peroxisome proliferator receptor-γ coactivator-1-alpha (PGC-1α) and uncoupling protein 2 (UCP2) content were measured. After eight weeks, chronic endurance exercise reduced GIIS in a dose-response manner proportionally to weekly exercise frequency. Contrariwise, an increase in GLUT2 protein content, CaMKII and AMPK phosphorylation levels was observed. These alterations were accompanied by an increase in uncoupling protein 2 (UCP2) content, probably mediated by an enhancement in PGC-1 α protein expression. In conclusion, chronic endurance exercise induces adaptations in β-cells leading to a reduction in GIIS, probably by activating the AMPK signaling pathway.
Vivian Calegari; Claudio Cesar Zoppi; Luiz Rezende; Leonardo Silveira; Everardo Carneiro; Antonio Carlos Boschero
Related Documents :
6742304 - Hamstring/quadriceps ratios in college football players: a high velocity evaluation.
11427364 - Does computer game play aid in motivation of exercise and increase metabolic activity d...
12740744 - Tennis, incidence of urti and salivary iga.
6525754 - Seasonal fluctuations of force production in high jumpers.
18392844 - Postactivation potentiation of short tetanic contractions is differently influenced by ...
12023864 - An acetyl group deficit limits mitochondrial atp production at the onset of exercise.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-1-6
Journal Detail:
Title:  The Journal of endocrinology     Volume:  -     ISSN:  1479-6805     ISO Abbreviation:  -     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-1-7     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375363     Medline TA:  J Endocrinol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
V Calegari, Physiology, UNICAMP, Campinas, Brazil.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Effects of cortisol and thyroid hormone on peripheral outer ring deiodination and osmoregulatory par...
Next Document:  Correction of Hyperglycemia in Type 1 Diabetic Models by Transplantation of Encapsulated Insulin-pro...