Deletion of Kinin B2 Receptor Alters Muscle Metabolism and Exercise Performance

Author(s):Show less -

Reis, Felipe C. G. ^[1] ; Haro, Anderson S. ^[1] ; Bacurau, Aline V. N. ^[2] ; Hirabara, Sandro M. ^[3] ; Wasinski, Frederick ^[1] ; Ormanji, Milene S. ^[4] ; Moreira, Jose B. N. ^[5] ; Kiyomoto, Beatriz H. ^[6] ; Bertoncini, Clelia R. A. ^[4] ; Brum, Patricia C. ^[2] ; Curi, Rui ^[3] ; Bader, Michael ^[7] ; Bacurau, Reury F. P. ^[8] ; Pesquero, Joao B. ^[1] ; Araujo, Ronaldo C. ^[1]

Affiliation

^[1] Univ Fed Sao Paulo, Dept Biophys, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Sch Phys Educ & Sport, Sao Paulo - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Sao Paulo - Brazil

^[4] Univ Fed Sao Paulo, CEDEME, Sao Paulo - Brazil

^[5] Norwegian Univ Sci & Technol NTNU, KG Jebsen Ctr Exercise Med, Trondheim - Norway

^[6] Univ Fed Sao Paulo, Dept Neurol & Neurosurg, Sao Paulo - Brazil

^[7] Max Delbruck Ctr Mol Med MDC, Berlin - Germany

^[8] Univ Sao Paulo, Sch Arts Sci & Humanities, Sao Paulo - Brazil

• Document type: Journal article
• Source: PLoS One; v. 10, n. 8 AUG 24 2015.
• Web of Science Citations: 5

Abstract

Metabolic syndrome is a cluster of metabolic risk factors such as obesity, diabetes and cardiovascular diseases. Mitochondria is the main site of ATP production and its dysfunction leads to decreased oxidative phosphorylation, resulting in lipid accumulation and insulin resistance. Our group has demonstrated that kinins can modulate glucose and lipid metabolism as well as skeletal muscle mass. By using B2 receptor knockout mice (B2R(-/-)) we investigated whether kinin action affects weight gain and physical performance of the animals. Our results show that B2R(-/-) mice are resistant to high fat diet-induced obesity, have higher glucose tolerance as well as increased mitochondrial mass. These features are accompanied by higher energy expenditure and a lower feed efficiency associated with an increase in the proportion of type I fibers and intermediary fibers characterized by higher mitochondrial content and increased expression of genes related to oxidative metabolism. Additionally, the increased percentage of oxidative skeletal muscle fibers and mitochondrial apparatus in B2R(-/-) mice is coupled with a higher aerobic exercise performance. Taken together, our data give support to the involvement of kinins in skeletal muscle fiber type distribution and muscle metabolism, which ultimately protects against fat-induced obesity and improves aerobic exercise performance. (AU)

• FAPESP's process: 13/04757-9 - Role of physical training in fetal reprogramming: emphasis on obesity
• Grantee: Ronaldo de Carvalho Araújo
• Support type: Regular Research Grants
• FAPESP's process: 08/06676-8 - Cellular and molecular biology of the kallikrein-kinin and renin-angiotensin systems
• Grantee: João Bosco Pesquero
• Support type: Research Projects - Thematic Grants