In human and ovine fetuses, glucocorticoids stimulate leptin secretion, although the extent to which leptin mediates the maturation effects of glucocorticoids on pulmonary development is unclear. This study investigated the effects of leptin administration on indices of lung structure and function before birth. Chronically-catheterised singleton sheep fetuses were infused i.v. for 5 days with either saline or recombinant ovine leptin (0.5 mg/kg/day, 0.5 LEP or 1.0 mg/kg/day, 1.0 LEP) from 125 days of gestation (term ∾145 days). Over the infusion, leptin administration increased plasma leptin, but not cortisol, concentrations. On the fifth day of infusion, 0.5 LEP reduced alveolar wall thickness and increased the volume at closing pressure of the pressure-volume deflation curve, inter-alveolar septal elastin content, secondary septal crest density and the mRNA abundance of the leptin receptor (Ob-R) and surfactant protein B. Neither treatment influenced static lung compliance, maximal lung volume at 40 cmH2O, lung compartment volumes, alveolar surface area, pulmonary glycogen, protein content of the long form signalling Ob-Rb or phosphorylated signal transducers and activators of transcription-3 (pSTAT3), or mRNA levels of surfactant proteins A, C or D, elastin, vascular endothelial growth factor (VEGF)-A, the VEGF receptor 2, angiotensin-converting enzyme (ACE), peroxisome proliferator- activated receptor γ (PPARγ) or parathyroid hormone-related peptide (PTHrP). Leptin administration in the ovine fetus during late gestation promotes aspects of lung maturation, including upregulation of surfactant protein B.