**1. Introduction**

Leptin, the product of *ob* (*obese*) gene, is a 16 kDa non-glycosylated polypeptide anti-obesity hormone mainly produced and secreted by adipose tissues [1]. Recent studies have demonstrated that leptin is also produced by placenta [2], stomach [3], skeletal muscles [4], brain, and pituitary gland [5, 6]. Leptin influences body weight homeostasis through its effects on food intake and

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

energy expenditure by negative feedback at the hypothalamic nuclei [7]. Leptin is also known to exhibit a variety of physiological actions on lipid metabolism [8], hematopoiesis [9], thermogenesis [10], ovarian function [11], bone formation [12, 13], and angiogenesis [14, 15]. The leptin receptor (Ob-R) is expressed in various tissues including the hypothalamus [16, 17], adipose tissue [18], skeletal muscle [19], and hepatocytes [18, 20]. The multifunctionality of leptin and the wide distribution of its receptor suggest that leptin plays a variety of physiological roles not only as a systemic hormone but also as a local growth factor.

The surface of the body is covered by skin to communicate with the external environment and to protect deeper tissues and organs by separating them from the external environment such as chemical, mechanical, and thermal stresses, infections, and dehydration [21, 22]. Normal dermal wound repair processes, such as inflammation, angiogenesis, contraction, deposition of extracellular matrix, granulation tissue formation, epithelialization, and remodeling, require various cellular and molecular signals [23]. In this biological process, skin fibroblasts interact with surrounding cells such as keratinocytes, inflammatory cells, and endothelial cells [21, 24]. Fibroblasts produce extracellular matrix, glycoproteins, adhesive molecules, and various cytokines [25, 26]. The lack of these signals may result in poor healing of wounds such as diabetic ulcers [27, 28].

A certain study showed that skin wound healing delayed in leptin deficient *ob/ob* mice and that exogenously administered leptin restored this delayed wound healing by enhancing reepithelialization of the wound in these mice in diabetic condition [29]. Another some studies unveiled the effect of leptin on wound healing by demonstrating that leptin acted as an autocrine/paracrine regulator in the wounded site [30, 31]. These findings strongly suggest the possibility that leptin could be a potential medicine for promoting wound healing in skin. However, all previous studies refer to whole-body dosage administered intraperitoneally, and even when administered locally, the leptin must have been administered every day. So, we investigated whether local and single-dose administration of leptin exerted a promotive influence on the skin wound healing. Because, we thought that local and single administration of leptin could avoid the influence of its adverse effect such as metabolic disorders, hyper/ hypoglycemia caused by the fact that leptin is a multifunctional and potent systemic hormone, and could be advantageous for the lowering of patients' distress in some cases in its clinical application.
