Role of Beta 3 Adrenergic Receptor in Facultative Thermogenesis

Abstract

Obesity, characterized by an increase in body fat, is related to a defect in facultative thermogenesis (FT). Brown adipose tissue (BAT) is the main site of this FT and is activated by Sympathetic Nervous System through the release of norepinephrine (NE) that binds to Beta adrenergic receptors (B‐ADR). Our goal was to evaluate the role of B3 isoform of B‐ADR in diet and cold‐induced FT. B3 knockout mice (KOB3) kept their body temperature normal when exposed to cold (4°C) and BAT thermogenic capacity was also normal when stimulated by NE i.v. infusion. In spite of a normal BAT activity, the absence of B3 receptor worsens diet‐induced obesity, with body weight gain significantly higher in KOB3 when compared to wild‐type (WT) mice (16g ± 1,4 vs. 12g ± 3,7) and larger epididymal adipocytes area (13079,81μm2 ± 10611,7 vs. 4501,55μm2 ± 1996,61). Also, a significant macrophages and neutrophils infiltration was observed in white adipose tissue (WAT), indicating inflammatory process in this tissue. Our results suggest that B3 receptor is not important in cold induced FT but it is fundamental to regulation of the body weight. It also indicates that this isoform mediates NE induced lipolysis since its absence results in very large adipocytes and inflammation in WAT.Supported by CAPES.