WAT and BAT, the two major fat tissues are found different morphologically and functionally in mammals (Wu et al., 2015). Specifically, WAT is mainly responsible for energy storage and BAT is mainly for thermoregulation i.e., to dissipate chemical energy in the form of heat (Wu et al., 2015). While WAT is traditionally known as the biggest mammalian triacylglycerol storage depot, recent studies suggest that WAT can be rendered brown-like features in response to certain stimulus (Jeremic et al., 2016). Remodeling of WAT is characterized by up-regulation of the BAT-specific gene Ucp1 and therefore exerts an energy-disposal capacity (Wu et al., 2015; Jeremic et al., 2016). Central infusion of GLP-1 was reported to stimulate BAT thermogenesis (Lockie et al., 2012; Beiroa et al., 2014; Kooijman et al., 2015). However, the role of peripheral GLP-1R activation in regulating energy expenditure remains controversial (Beiroa et al., 2014). Our observations that chronic peripheral treatment with the novel GLP-1R agonist supaglutide upregulated the expression of Ucp1 in inguinal WAT, but not in BAT or epididymal WAT, suggesting increase in UCP1-containing adipocytes (Petrovic et al., 2010) or beige adipocytes (Wu et al., 2012) upon supaglutide treatment. It is conceivable that supaglutide-induced anti-obesity effect was at least in part contributed by the browning of inguinal WAT, rather than activated BAT thermogenesis. Mechanistic analysis in the context of white browning phenotype in supaglutide treated mice is clearly warranted for future study. However, our data is supported by others' studies which demonstrated that liraglutide treatment did not affect BAT thermogenesis, but significantly reduced body weight and adiposity in obese mice (Heppner et al., 2015), implying that there is additional physiological mechanism underlying the effect of GLP-1R agonists on weight reduction. Nevertheless, it is possible that supaglutide treatment altered the adipose tissue heterogeneity i.e., changes in depot-specific differences may give rise to different metabolic consequences under obese condition (Rosell et al., 2014; Kwok et al., 2016).