The high prevalence of obesity has provoked substantial interest in adipocyte thermogenesis. Several studies have revealed functional BAT in adult humans, and have demonstrated inducible brite (brown in white) adipocytes in animal models by multiple stimuli including the PPARγ activator rosiglitazone. Brite adipocytes are characterised by expression of the uncoupling protein UCP1 and although derived from a white adipocyte lineage, they express the brown adipocyte transcriptional co-regulator Prdm16. We determined the effect of rosiglitazone on β-adrenoceptor function (assessed by oxygen consumption rates (Seahorse XF96), cyclic AMP assays, glucose uptake assays) in primary mouse adipocytes from interscapular BAT and inguinal WAT (iWAT). OCR, cyclic AMP and glucose uptake responses were absent-minimal from control iWAT cultures but were markedly induced in rosiglitazone-treated cells. Preliminary experiments investigating the in vivo effect of rosiglitazone on β-adrenoceptor function was assessed using whole body oxygen consumption and in vivo glucose uptake, which showed a trend for increased β-adrenoceptor function in vivo. These studies suggest that cells from iWAT undergo rosiglitazone-induced brite differentiation and have the capacity for increased thermogenesis via UCP1 activation, which may be of significance in vivo.