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.
Highlights
The kallikrein-kinin system (KKS) is a multi-enzymatic system in which function is mediated by the interaction of peptides called kinins with two different G-protein-coupled receptors, B1 and B2 (B1R and B2R, respectively)
We showed that B2R regulates skeletal muscle mass by altering myostatin gene expression [21]
We hypothesized that B2R could have a role in metabolic disorders and physical performance and submitted B2R-/- mice to a high fat diet treatment and physical tests
Summary
The kallikrein-kinin system (KKS) is a multi-enzymatic system in which function is mediated by the interaction of peptides called kinins with two different G-protein-coupled receptors, B1 and B2 (B1R and B2R, respectively). Initial evidences regarding a potential involvement of KKS with skeletal muscle (SM) metabolism were reported two decades ago; muscle blood flow and skeletal muscle glucose uptake can be modulated by bradykinin via the constitutively expressed B2 receptor [3,4,5]. Absence of B2R resulted in lower tissue sensitivity to insulin and glucose uptake [6]. We demonstrated that B2R-/- mice presented increased postnatal protein body mass, gastrocnemius mass and decreased expression of myostatin in gastrocnemius in postnatal period in comparison to WT counterparts [7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
