Affiliation:
1. Unidad de Investigación en Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, 54090 Estado de México, México
2. Departamento de Farmacología, Instituto Nacional de Cardiología “Ignacio Chávez”, Tlalpan, 14080 Ciudad de México, México
Abstract
Abstract
A single bout of exercise increases subsequent insulin-stimulated glucose uptake in skeletal muscle; however, it is unknown whether angiotensin-(1-7) (Ang-(1-7)), a vasoactive peptide of the renin-angiotensin system, participates in this process. The aim of this study was to investigate the possible involvement of Ang-(1-7) in enhanced skeletal muscle insulin sensitivity after an exercise session. Male Wistar rats were forced to swim for 2.5 hours. Two hours after exercise, insulin tolerance tests and 2-deoxyglucose uptake in isolated soleus muscle were assessed in the absence or presence of the selective Mas receptor (MasR, Ang-(1-7) receptor) antagonist A779. Ang II and Ang-(1-7) levels were quantified in plasma and soleus muscle by HPLC. The protein abundance of angiotensin-converting enzyme (ACE), ACE2, Ang II type 1 receptor (AT1R), and MasR was measured in soleus muscle by Western blot. Prior exercise enhanced insulin tolerance and insulin-mediated 2-deoxyglucose disposal in soleus muscle. Interestingly, these insulin-sensitizing effects were abolished by A779. After exercise, the Ang-(1-7)/Ang II ratio decreased in plasma, whereas it increased in muscle. In addition, exercise reduced ACE expression, but it did not change the protein abundance of AT1R, ACE2, and MasR. These results suggest that Ang-(1-7) acting through MasR participates in enhanced insulin sensitivity of skeletal muscle after a bout of exercise.
Funder
PAPIIT-DGAPA
Universidad Nacional Autónoma de México
Subject
Endocrinology, Diabetes and Metabolism
Cited by
17 articles.
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