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Adiponectin is one of the most effective adipokines in the context of correcting obesity-induced insulin resistance. However, adiponectin-deficient animal models show a relatively modest phenotype unless metabolically challenged. This suggests that potent compensatory mechanisms are in place. In this issue of the Biochemical Journal, Wong et al. characterize new members of the CTRPs [C1q-TNFα (tumour necrosis factor α)-related proteins]. They establish that some CTRPs are produced primarily in the stromal vascular fraction of adipose tissue, and that expression of CRTP1, in particular (like adiponectin), is induced by PPARγ (peroxisome-proliferator-activated receptor γ) agonists. Moreover, injection of recombinant CTRP1 displays glucose-lowering effects. These observations suggest that CTRP1 may have partially overlapping functions and, along with other paralogues, may effectively compensate for the chronic loss of adiponectin function. [ABSTRACT FROM AUTHOR]