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In diabetic patients impaired wound healing conditions are a therapeutic problem of clinical importance. Recently, we showed that supplemented leptin induced an acceleration of impaired wound closure in diabetic ob/ob mice by reversion of the delayed re-epithelialization process. Additionally, angiogenesis is central to a normal repair. As leptin has been reported to represent an angiogenic factor, we hypothesized that leptin-mediated angiogenic processes at the wound site might participate in leptin-mediated improvement of disturbed repair in ob/ob mice.

Systemically and topically supplemented leptin fails to reconstitute a normal angiogenic response during skin repair in diabetic ob/ob mice