Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/235970
Type: Artigo de periódico
Title: Endurance Training Inhibits Insulin Clearance And Ide Expression In Swiss Mice.
Author: Costa-Júnior, José M
Ferreira, Sandra M
Protzek, André O
Santos, Gustavo J
Cappelli, Ana P
Silveira, Leonardo R
Zoppi, Cláudio
de Oliveira, Camila A M
Boschero, Antonio C
Carneiro, Everardo M
Rezende, Luiz F
Abstract: Endurance training improves peripheral insulin sensitivity in the liver and the skeletal muscle, but the mechanism for this effect is poorly understood. Recently, it was proposed that insulin clearance plays a major role in both glucose homeostasis and insulin sensitivity. Therefore, our goal was to determine the mechanism by which endurance training improves insulin sensitivity and how it regulates insulin clearance in mice. Mice were treadmill-trained for 4 weeks at 70-80% of maximal oxygen consumption (VO2 max) for 60 min, 5 days a week. The glucose tolerance and the insulin resistance were determined using an IPGTT and an IPITT, respectively, and the insulin decay rate was calculated from the insulin clearance. Protein expression and phosphorylation in the liver and the skeletal muscle were ascertained by Western blot. Trained mice exhibited an increased VO2 max, time to exhaustion, glucose tolerance and insulin sensitivity. They had smaller fat pads and lower plasma concentrations of insulin and glucose. Endurance training inhibited insulin clearance and reduced expression of IDE in the liver, while also inhibiting insulin secretion by pancreatic islets. There was increased phosphorylation of both the canonical (IR-AKT) and the non-canonical (CaMKII-AMPK-ACC) insulin pathways in the liver of trained mice, whereas only the CaMKII-AMPK pathway was increased in the skeletal muscle. Endurance training improved glucose homeostasis not only by increasing peripheral insulin sensitivity but also by decreasing insulin clearance and reducing IDE expression in the liver.
Citation: Plos One. v. 10, n. 3, p. e0118809, 2015.
Rights: aberto
Identifier DOI: 10.1371/journal.pone.0118809
Address: http://www.ncbi.nlm.nih.gov/pubmed/25822220
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

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