The adiposity hormone leptin regulates food intake, body weight, reproduction and other metabolic and endocrine functions mainly through signaling to the hypothalamus. Leptin signaling to peripheral tissues other than the hypothalamus has been suggested for a number of processes such as immunity, bone metabolism, hematopoiesis, angiogenesis, and wound healing. It was previously shown that exogenously applied leptin accelerated wound healing and that leptin mRNA is expressed at the wound site, but there is no published evidence showing that it is translated into leptin protein that is available at the site of repair. To address this question we analyzed pig wound fluids collected from partial-thickness excisional wounds during the first 9 days after injury. Leptin was measured using a modified culture of HEK-293 cells, expressing both the human leptin receptor gene and the firefly luciferase gene driven by a STAT-inducible promoter. Relatively high levels of leptin activity (50-250 ng/ml) were detected in wound fluids using the leptin receptor expressing HEK-293 cells. Our results suggest that leptin is normally induced (4.8- to 10.2-fold) in wound tissue during the first few days following injury and may operate in a paracrine or autocrine circuit during the wound repair process.