Calcifediol Treatment Improves Skin Wound Healing in Vitamin D Deficiency Obese Rats

Background/Objectives: Obesity is a major public health problem and a risk factor for numerous diseases. Furthermore, the high prevalence of 25-hydroxyvitamin D (25(OH)D) deficiency in obese individuals promotes a state of persistent inflammation and contributes to the development of hard-to-heal skin wounds. Although calcifediol is effective in correcting this deficiency, its effect on cutaneous wound healing in obesity has not been fully established. Thus, the objective of this work has been to evaluate the impact of calcifediol treatment on wound healing in an animal model of obesity with vitamin D deficiency. Methods: Wistar rats fed a high-fat, vitamin D-deficient diet were subjected to dorsal skin wounds. One group received calcifediol treatment for 14 days. Serum 25(OH)D levels, wound closure rate, histological parameters, and molecular markers related to inflammation were analyzed. Results: Calcifediol significantly increased serum 25(OH)D levels and accelerated wound closure compared to untreated animals. It also improved re-epithelialization, reduced the depth and extent of the lesions, and promoted collagen deposition. Furthermore, it increased the expression of anti-inflammatory markers (IL-10 and CD163) and decreased the infiltration of CD68+ macrophages, indicating a more efficient resolution of the inflammatory response. Conclusions: Calcifediol supplementation improves cutaneous wound healing in obesity with 25(OH)D deficiency by accelerating wound closure, promoting extracellular matrix remodeling, and modulating the inflammatory response, supporting its use as a complementary strategy to enhance tissue repair in conditions of obesity and vitamin D deficiency.