School of Podiatric Medicine - Student Research

Document Type

Poster

Publication Date

2025

Abstract

Introduction and Hypothesis: The aim of this study is to compare soft tissue morphology and fibrosis pathology of different organs between diabetic and non-diabetic rats. Type 2 diabetes causes soft tissue remodeling in organ systems including heart, kidney, spleen, and pancreas. Fibrotic remodeling is a common pathological mechanism seen in diabetes-related organ dysfunction. By understanding fibrotic pathology in rats, it serves as a foundation to develop lower limb models applicable to podiatry. These systemic changes caused by diabetes may also play a role in lower limb changes such as diabetic ulcers and delayed wound healing.

Methodology: Male Lewis rats (6 weeks old) were assigned to two different groups: diabetic (D) or non-diabetic (ND) (n=6). Diabetes was induced via high-fat diet (HFD) for 6 weeks followed by an intraperitoneal injection of streptozotocin (STZ, 55 mg/kg). Streptozotocin is toxic to beta cells which produce insulin, causing the rats to become insulin deficient. ND controls received a normal diet and intraperitoneal injection of saline solution. After 48 hours of STZ injection, and confirmation of diabetes, rats were treated with HFD until euthanasia for sample collection. After 28 days of STZ (D group) or saline injection (ND group), different organ tissues were harvested, fixed and processed into 5 μm slices. H&E was done to assess general tissue morphology. Picrosirius red (PSR) was done to visualize collagen and fibrosis development.

Results: In D group, the heart revealed thickened coronary arteries with periarterial fibrosis. The myocardium had fewer intercalated discs. Also, there was a significant increase in PSR signaling in coronary branches and myocardium, indicating early signs of fibrosis. The kidney showed milder signs of fibrosis, but H&E staining revealed disrupted glomeruli, atrophic tubules, and focal arteriolar hyalinosis. In the spleen, D rats had reduced white pulp and blurred boundaries between red and white pulp. For the pancreas, D group had reduced islet size, indicating beta cell loss. For the spleen and pancreas, D group also showed milder signs of fibrosis.

Discussion and Conclusion: Diabetes induction resulted in morphological alterations in the soft tissue of various organs. All organs showed structural damage and cellular atrophy. Notably, there was a significant increase of fibrosis in coronary arteries and pericardium. These results highlight the cellular changes and fibrotic remodeling caused by early diabetes. Future studies will focus on how early diabetes affect soft tissue in lower limbs in comparison to soft tissue in organs. Additionally, this study will explore how fibrosis may contribute to complications in lower extremities, such as ulcers and delayed wound healing.

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