Angiotensin-(1-7), Adipokines and Inflammation

Nowadays the adipose tissue is recognized as one of the most critical endocrine organs releasing many adipokines that regulate metabolism, inflammation and body homeostasis. There are several described adipokines, including the renin-angiotensin system (RAS) components that are especially activated...

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Veröffentlicht in:Metabolism, clinical and experimental clinical and experimental, 2019-06, Vol.95, p.36-45
Hauptverfasser: Lelis, Deborah de Farias, Freitas, Daniela Fernanda de, Machado, Amanda Souto, Crespo, Thaísa Soares, Santos, Sérgio Henrique Sousa
Format: Artikel
Sprache:eng
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Zusammenfassung:Nowadays the adipose tissue is recognized as one of the most critical endocrine organs releasing many adipokines that regulate metabolism, inflammation and body homeostasis. There are several described adipokines, including the renin-angiotensin system (RAS) components that are especially activated in some diseases with increased production of angiotensin II and several pro-inflammatory hormones. On the other hand, RAS also expresses angiotensin-(1–7), which is now recognized as the main peptide on counteracting Ang II effects. New studies have shown that increased activation of ACE2/Ang-(1–7)/MasR arm can revert and prevent local and systemic dysfunctions improving lipid profile and insulin resistance by modulating insulin actions, and reducing inflammation. In this context, the present review shows the interaction and relevance of Ang-(1–7) effects on regulating adipokines, and as one adipokine itself, modulating body homeostasis, with emphasis on its anti-inflammatory properties, especially in the context of metabolic disorders with focus on obesity and type 2 diabetes mellitus pandemic. •The white adipose tissue secretes several bioactive molecules called adipokines.•The adipokines exert local and systemic effects on metabolism.•The angiotensin-(1–7) modulates the adipokines.•Inflammation is modulated by adipokines, and angiotensin-(1–7).
ISSN:0026-0495
1532-8600
DOI:10.1016/j.metabol.2019.03.006