Abstract
Leptin mimics many of the antidiabetic actions of insulin in insulin-deficient diabetes, but the mechanism is controversial. Fujikawa et al. (2013) reveal that leptin receptors in γ-aminobutyric acid (GABA)-ergic and pro-opiomelanocortin (POMC) neurons in the central nervous system are sufficient to mediate the lifesaving and antidiabetic actions of leptin in insulin-deficient mice.