Evidence mapPaperPMID 41947182Full record

ArticleJournal of diabetes investigation2026

Effects of imeglimin on experimental diabetic neuropathy in streptozotocin-induced diabetic rats.

Wataru Nihei, Ayako Kato, Takuma Sato, Masahiro Yamaguchi, Tatsuhito Himeno, Nobuhisa Nakamura, Kazunori Sango, Keiko Naruse, Jiro Nakamura, Hideki Kamiya and 1 more

Abstract read
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Article in Journal of diabetes investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Wataru Nihei *Laboratory of Medicine, Aichi Gakuin University School of Pharmacy, Nagoya, Aichi, Japan.ORCID https://orcid.org/0000-0002-3073-5118
Ayako Kato *Laboratory of Medicine, Aichi Gakuin University School of Pharmacy, Nagoya, Aichi, Japan.
Takuma SatoLaboratory of Medicine, Aichi Gakuin University School of Pharmacy, Nagoya, Aichi, Japan.
Masahiro YamaguchiDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
Tatsuhito HimenoDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
Nobuhisa NakamuraDepartment of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya, Aichi, Japan.ORCID https://orcid.org/0000-0003-3265-5194
Kazunori SangoDiabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.ORCID https://orcid.org/0000-0002-9750-9596
Keiko NaruseDepartment of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya, Aichi, Japan.ORCID https://orcid.org/0000-0002-0062-0694
Jiro NakamuraTDE Healthcare Corporation TOSAKI Meito Clinic for Diabetes and Endocrinology, Nagoya, Aichi, Japan.
Hideki KamiyaDivision of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.ORCID https://orcid.org/0000-0003-3197-2542
Koichi KatoLaboratory of Medicine, Aichi Gakuin University School of Pharmacy, Nagoya, Aichi, Japan.

Funding

Japan Society for the Promotion of Science 21K06718
6 · The paper itself

Abstract

AIMS/

introductionAs a common chronic complication, diabetic neuropathy affects a substantial number of individuals with diabetes mellitus, with limited therapeutic options addressing the underlying pathogenesis. The glucose-lowering action of imeglimin is mediated through improved insulin sensitivity in peripheral organs, including the skeletal muscle and liver, along with augmented insulin release from β-cells. Imeglimin exerts its effects in part by modulating mitochondrial complex I, leading to the reduced production of reactive oxygen species and protection against metabolic stress. Despite these beneficial effects, the effect of imeglimin on diabetic neuropathy remains unclear. In this study, we evaluated whether imeglimin ameliorated peripheral nerve dysfunction in streptozotocin (STZ)-induced diabetic rats. MATERIALS AND

methodsThe rats received imeglimin (200 mg/kg twice daily) or vehicle for 4 weeks, and the sensory nerve conduction velocity (SNCV), motor nerve conduction velocity (MNCV), sciatic nerve blood flow (SNBF), and intraepidermal nerve fiber density (IENFD) were assessed. Neurite outgrowth was examined in ND7/23 cells derived from the dorsal root ganglion.

resultsImeglimin treatment significantly improved SNCV, SNBF, and IENFD without affecting blood glucose levels, indicating neuroprotective effects, independent of glycemic control. Furthermore, imeglimin enhanced neurite outgrowth in ND7/23 cells, demonstrating its direct neurotrophic effect. These findings indicate that imeglimin protects against diabetic neuropathy by enhancing nerve blood flow and promoting neurite growth independent of the systemic control of glycemia.

conclusionsThis study provides supporting evidence for the potential therapeutic application of imeglimin in diabetic neuropathy.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NeuropathiesTriazinesAnimalsBlood GlucoseGanglia, SpinalMaleNerve Conduction StudiesNeural ConductionRatsRats, Sprague-DawleySciatic NerveStreptozocinBlood GlucoseimegliminStreptozocinTriazinesdiabetes mellitusdiabetic neuropathyimeglimin

Identifiers

PMID41947182
PMCPMC13238588

What Socratic holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.