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A lack of murine models that mimic impaired wound healing in people with type 2 diabetes has hindered research. The commonly used leptin-receptor knockout model (db/db) fails to accurately reflect the pathophysiology of human disease. This study aimed: (i) to investigate whether our novel murine model of diabetes, whilst less hyperglycaemic and obese than db/dbs, effectively demonstrated impaired wound healing, and (ii) to identify the most robust methods for quantifying wound closure. C57BL/6J mice were high-fat diet fed for a total of 11 weeks and injected with three doses of streptozotocin (65 mg/kg body weight) at week 5 with chow-fed mice as controls. All mice received four excisional wounds and were euthanised at day-4 or day-10 post-wounding (n = 8/group/timepoint). Wound healing was evaluated by digital planimetry, histology, Micro-CT, and tensiometry. Histological analysis was the most sensitive method for identifying impaired wound healing. Our high-fat diet/low-dose streptozotocin model had significantly higher non-fasting blood glucose (25.7 ± 5.4 mmol/L vs. 8.7 ± 0.8 mmol/L) and lower wound quality scores (day-4 post-wounding: 2.6 ± 1.9 vs. 4.4 ± 0.8) than healthy controls (both p < 0.05). At day-10 post-wounding, a linear trend in wound healing was observed between healthy controls, our novel model and the db/db model, indicating that our diabetic murine model may be clinically relevant for studying diabetes-related wound healing.
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