What is the mechanism underlying the turnover of β-adrenergic receptor on hypertrophied primary adipocytes?

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The purpose of the current study is to investigate the trafficking of β_2-adrenergic receptor (β_2-AR) can regulate the lipolysis in high fat diet-induced hypertrophied adipocytes (HA) that are observed in obese mammals. The animals (C57BL/6J mice) were randomly divided into two groups : a normal diet intake and high fat diet intake, and adipocytes were isolated from epididymal adipose tissue. Low concentration (10 nM) of Isoproterenol (ISO)-stimulated lipolysis was significantly elevated in HA than that in non hypertrophied control (NHC) cells. In contrast, lipolysis in HA was significantly attenuated in high concentration (1 μM) of ISO compared with NHC. Under this condition, in membrane fraction, the levels of β_2-AR was significantly reduced in HA compared with NHC, accompanied by increased levels of β-arrestin-2 and β_2-AR/β-arrestin-2 complex, which are accelerator of agonist-induced trafficking of the β_2-AR from plasma membrane to cytosol. These results suggest that trafficking i.e., internalization of β_2-AR, with high concentration of ISO would be associated with reduced levels of lipolytic response in HA, and that this phenomenon is one of the mechanism underlying lower levels of fatmetabolism in obese mammals in vivo.