School of Podiatric Medicine - Student Research

Document Type

Poster

Publication Date

2026

Abstract

Introduction/Purpose: Type 2 diabetes and obesity are major risk factors for delayed wound healing in chronic foot ulcers. This study investigated whether a high-fat diet induces diabetes-like metabolic dysfunction in mice and characterized associated morphological changes and macrophage polarization during wound healing. Macrophages exist as pro-inflammatory M1 and anti-inflammatory M2 phenotypes that regulate tissue repair.

Methods: Ten male C57BL/6J mice (8 weeks old) were divided into high-fat diet (HFD) and regular diet (RD) (IACUC Protocol 22-33) groups.  After 12 weeks, body weight and intraperitoneal glucose tolerance test were measured to confirm metabolic phenotypes, after which a 6mm dorsal excision wound was created. Mice were euthanized 7 days later, and tissue samples were analyzed by H&E and immunofluorescence for macrophage polarization into M1 (CD80) or M2 (CD163).

Results: HFD mice exhibited significantly greater body weight and elevated blood glucose levels compared with RD mice, confirming diet-induced metabolic dysfunction. Although no statistically significant difference in wound closure was observed between the groups, RD mice demonstrated a trend toward greater wound closure. Histological evaluation by H&E staining revealed multiple, larger, and well-defined vacuolated spaces within the granulation tissue/deep wound bed of HFD mice, consistent with adipose tissue dropout. Qualitative immunofluorescence demonstrated M1 macrophage expression in both RD and HFD groups, whereas M2 macrophage expression appeared more abundant in RD mice.

Conclusion: HFD induced metabolic dysfunction with increased inflammation and adipose tissue consistent with impaired wound healing. Increased M1 polarization with relative M2 enrichment in RD suggests delayed repair in HFD and pro-regenerative activity in RD.

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