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Hypoadiponectinemia and adiponectin resistance are implicated in the aetiology of obesity-related cardiometabolic disorders, hence represent a potential therapeutic axis. Here we characterised the effects of  in vivo  electrotransfer-mediated overexpression of the adiponectin receptors, AdipoR1 or AdipoR2, into tibialis anterior muscle (TAM) of lean or obese mice. In lean mice, TAM-specific overexpression of AdipoR1 ( TAM R1) or AdipoR2 ( TAM R2) increased phosphorylation of AMPK, AKT and ERK and expression of the insulin responsive glucose transporter  glut4 . In contrast, only  TAM R2 increased  pparα  and a target gene  acox1 . These effects were decreased in obese mice despite no reduction in circulating adiponectin levels.  TAM R2 also increased expression of  adipoQ  in TAM of lean and obese mice. Furthermore, in obese mice  TAM R2 promoted systemic effects including; decreased weight gain; reduced epididymal fat mass and inflammation; increased epididymal  adipoQ  expression; increased circulating adiponectin. Collectively, these results demonstrate that AdipoR1 and AdipoR2 exhibit overlapping and distinct effects in skeletal muscle consistent with enhanced adiponectin sensitivity but these appear insufficient to ameliorate established obesity-induced adiponectin resistance. We also identify systemic effects upon  TAM R2 in obese mice and postulate these are mediated by altered myokine production. Further studies are warranted to investigate this possibility which may reveal novel therapeutic approaches.

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Muscle-specific overexpression of AdipoR1 or AdipoR2 gives rise to common and discrete local effects whilst AdipoR2 promotes additional systemic effects