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Histological and Functional Changes Induced by Compression and Decompression Develop Slower in Diabetic Nerves Than in Nondiabetic Nerves
Journal article   Open access   Peer reviewed

Histological and Functional Changes Induced by Compression and Decompression Develop Slower in Diabetic Nerves Than in Nondiabetic Nerves

Ignacio Garcia Fleury, Jessica E Goetz, Douglas C Fredericks, Emily B Petersen, Natalie A Glass and Joseph A Buckwalter
BioMed research international, Vol.2026, e3777921
09/10/2026
DOI: 10.1155/bmri/3777921
PMCID: PMC13563056
PMID: 42723366
url
https://doi.org/10.1155/bmri/3777921View
Published (Version of record) Open Access

Abstract

Treatment of compressive neuropathies in diabetic patients remains controversial, with variable functional outcomes reported. This study is aimed at establishing a rat model of diabetic nerve compression that is suitable for investigations of diabetic nerve recovery after surgical decompression. Twenty male Zucker diabetic fatty obese (diabetic) and 20 lean (nondiabetic) rats underwent surgery to compress the sciatic nerve using a polymer sleeve or sham surgery. Six weeks later, decompression surgery or second sham surgery was performed. Nerve conduction velocities (NCV) and nociception via von Frey filaments (vF) were monitored weekly. Histological measures of nerve structure were compared between groups after 6 weeks of compression and 6 weeks after surgical decompression. Both diabetic and nondiabetic compressed nerves had significant reductions in NCV immediately postoperatively (p < 0.001) and progressive reductions in vF threshold during the compression period (p ≤ 0.002). After decompression, vF threshold and NCV increased; however, nerve function did not return to baseline or sham control values in either compressed group. Six weeks of compression significantly reduced axon size (p < 0.001) and myelin thickness (p = 0.014) in nondiabetic nerves but minimally changed the histological appearance of diabetic nerves. Decompression of nondiabetic nerves increased axon numbers (p = 0.005) but did not affect myelin thickness. In diabetic nerves, decompression also increased axon numbers, whereas myelin thickness decreased (p = 0.022) to levels similar to nondiabetic nerves. The histological response of nondiabetic nerves to compression and decompression was more pronounced than the functional response. Diabetic nerves showed a similar reaction to nondiabetic nerves but at a slower rate.
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