INS and metabolic syndrome: Yamauchi et al. (2007) reported that the AdipoR2-null mice exhibit similar phenotypes as mice lacking AdipoR1. Independently, two groups showed that AdipoR2-deficient mice are resistant to high-fat diet-induced obesity and dyslipidemia and exhibit markedly improved glucose tolerance, insulin sensitivity, physical activity, and energy expenditure: phenotypes that are the opposite to those observed in the AdipoR1 knockout mice (Bjursell et al., 2007; Liu et al., 2007).