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Nerve Injury and Regeneration · Journal article
The Faseb Journal · September 5, 2026
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This is a preclinical characterization of two polygenic mouse strains (RCS10 and TALLYHO/JngJ) that develop metabolic dysfunction and peripheral neuropathy by 24 weeks, with phenotypes reported to resemble human Type 2 diabetes-associated DPN more closely than existing models. A single uncontrolled calorie-restriction intervention in RCS10 mice showed restoration of large fiber function but not nerve fiber density, suggesting these may be useful for mechanistic studies and drug screening, but the work is exploratory and lacks rigorous experimental design or quantitative outcome reporting.
Preclinical model characterization with single-arm dietary intervention. NONcNZO10/LtJ (RCS10) and TALLYHO/JngJ (TH) polygenic mouse strains; enrollment criteria and numbers not specified.. Intervention: Calorie-restricted diet at 60% of standard intake for 8 weeks (RCS10 mice only).
Both RCS10 and TH strains developed obesity, hyperglycemia, dyslipidemia, and DPN by 24 weeks of age Hyperinsulinemia observed only in RCS10 mice Metabolic and neuropathic phenotypes of RCS10 and TH more closely resembled human DPN compared to monogenic and high-fat diet-induced models
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These models are positioned as tools for preclinical study of DPN mechanisms and drug screening, claimed to better recapitulate human disease than existing strains. However, the lack of quantitative efficacy data, sample sizes, and rigorous experimental design limits conclusions about the utility of the dietary intervention for translational research.
Characterization of two novel mouse models of diabetic peripheral neuropathy with metabolic and neuropathic phenotyping; uncontrolled intervention in one strain suggests feasibility but lacks comparison groups and human validation.
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These models are positioned as tools for preclinical study of DPN mechanisms and drug screening, claimed to better recapitulate human disease than existing strains. However, the lack of quantitative efficacy data, sample sizes, and rigorous experimental design limits conclusions about the utility of the dietary intervention for translational research.
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Diabetic peripheral neuropathy (DPN), a severe complication of Type 2 diabetes (T2D), is marked by progressive distal-to-proximal axonal degeneration. Although animal models have advanced our understanding of DPN pathogenesis, preclinical successes rarely translate into effective therapies, underscoring the need for models that more faithfully mirror human disease. In this study, we characterized two polygenic mouse strains, NONcNZO10/LtJ (RCS10) and TALLYHO/JngJ (TH), and found that both models developed obesity, hyperglycemia, dyslipidemia, and DPN by 24 weeks of age. However, hyperinsulinemia was observed only in RCS10 mice. Compared to monogenic and high-fat diet-induced models, the metabolic and neuropathic phenotypes of RCS10 and TH more closely resembled those of human DPN. In the second phase of the study, RCS10 mice were subjected to a calorie-restricted diet (60% of standard intake) for 8 weeks, which improved metabolic health and restored large fiber function, although intraepidermal nerve fiber density remained unchanged. Together, these findings identify RCS10 and TH mice as clinically relevant polygenic models for studying DPN pathogenesis and evaluating targeted therapeutic strategies.
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