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The DOI matches its Crossref record; 114 of the 114 references it cites were found in a registry or an index.

Redox imbalance stress in diabetes mellitus: Role of the polyol pathway

Open access
Yan, Liang‐jun·2018·Animal Models and Experimental Medicine

Abstract

In diabetes mellitus, the polyol pathway is highly active and consumes approximately 30% glucose in the body. This pathway contains 2 reactions catalyzed by aldose reductase (AR) and sorbitol dehydrogenase, respectively. AR reduces glucose to sorbitol at the expense of NADPH , while sorbitol dehydrogenase converts sorbitol to fructose at the expense of NAD + , leading to NADH production. Consumption of NADPH , accumulation of sorbitol, and generation of fructose and NADH have all been implicated in the pathogenesis of diabetes and its complications. In this review, the roles of this pathway in NADH / NAD + redox imbalance stress and oxidative stress in diabetes are highlighted. A potential intervention using nicotinamide riboside to restore redox balance as an approach to fighting diabetes is also discussed.

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Show all 114 references

Research works printed but not linked: 11

  1. 10.1152/ajpendo.00223.2007 · doi:10.1152/ajpendo.00223.2007
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  11. 10.1096/fj.03-0128fje · doi:10.1096/fj.03-0128fje

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Metadata

Authors
Yan, L.
Venue
Animal Models and Experimental Medicine
Publisher
Wiley
Published
2018-03
Volume
1
Issue
1
Pages
7-13
ISSN
  • 2096-5451 (ISSN-L)
  • 2576-2095
OpenAlex
W2800038406
Cited by
323
References
114
FWCI
11.35
Type
journal article
Language
en
Open access
gold
Funders
National Institutes of Health (R01NS079792)

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CoChat. (2026). Citation check: Redox imbalance stress in diabetes mellitus: Role of the polyol pathway. https://app.cochat.ai/papers/10.1002/ame2.12001
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Yan, L. (2018). Redox imbalance stress in diabetes mellitus: Role of the polyol pathway. Animal Models and Experimental Medicine. https://doi.org/10.1002/ame2.12001

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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