treated with FGF21. Additionally, the combination therapy of leptin and FGF21 improved all glucose and insulin measures (Figures 6A–D). The incremented effect in the GTT bore resemblance to that of the transplant + FGF21 group in the transplantation study (Figures 4H and 6D), suggesting that leptin, may be responsible for restoring part of the anti-diabetic efficacy of FGF21 in these mice. These data suggest WAT and leptin, but not liver dictate the anti-diabetic potential of FGF21. Consistent with this hypothesis is the finding that FGF21-induced signaling in the liver of lipodystrophic mice appears normal (Figure 3D).
