ArticleAntioxidants & redox signaling2010
Early neural and vascular dysfunctions in diabetic rats are largely sequelae of increased sorbitol oxidation.
Article in Antioxidants & redox signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Racial outcomes in patients with diabetic cardiomyopathy treated with an aldose reductase inhibitor: the ARISE-HF trial.Open heart · 2026Trial
- Tempol, a Superoxide Dismutase Mimetic, Inhibits Wallerian Degeneration Following Spinal Cord Injury by Preventing Glutathione Depletion and Aldose Reductase Activation.Journal of neurotrauma · 2024Article
- Cellular stress signaling and the unfolded protein response in retinal degeneration: mechanisms and therapeutic implications.Molecular neurodegeneration · 2022Review
- Epigenetic basis of diabetic vasculopathy.Frontiers in endocrinology · 2022Review
- Mitochondria in Diabetic Kidney Disease.Cells · 2021Review
- Aldose Reductase: An Emerging Target for Development of Interventions for Diabetic Cardiovascular Complications.Frontiers in endocrinology · 2021Review
- Role of the Polyol Pathway in Locomotor Recovery and Wallerian Degeneration after Spinal Cord Contusion Injury.Neurotrauma reports · 2021Article
- NADSignal transduction and targeted therapy · 2020Review
- Diabetic Retinopathy: The Role of Mitochondria in the Neural Retina and Microvascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Vitamin K1 prevents diabetic cataract by inhibiting lens aldose reductase 2 (ALR2) activity.Scientific reports · 2019Article
- Effects of Mitochondrial Dysfunction via AMPK/PGC-1 α Signal Pathway on Pathogenic Mechanism of Diabetic Peripheral Neuropathy and the Protective Effects of Chinese Medicine.Chinese journal of integrative medicine · 2019Review
- Redox imbalance and mitochondrial abnormalities in the diabetic lung.Redox biology · 2017Article
- Mitochondrial dysfunction in diabetic neuropathy: a series of unfortunate metabolic events.Current diabetes reports · 2015Review
- Roles of Pyruvate, NADH, and Mitochondrial Complex I in Redox Balance and Imbalance in β Cell Function and Dysfunction.Journal of diabetes research · 2015Review
- Aldose reductase, oxidative stress and diabetic cardiovascular complications.Cardiovascular & hematological agents in medicinal chemistry · 2012Review
- Impaired adenosine monophosphate-activated protein kinase signalling in dorsal root ganglia neurons is linked to mitochondrial dysfunction and peripheral neuropathy in diabetes.Brain : a journal of neurology · 2012Article
- Interplay of sorbitol pathway of glucose metabolism, 12/15-lipoxygenase, and mitogen-activated protein kinases in the pathogenesis of diabetic peripheral neuropathy.Biochemical pharmacology · 2012Article
- Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes.Mitochondrion · 2011Review
- Article
- Evaluation of the aldose reductase inhibitor fidarestat on ischemia-reperfusion injury in rat retina.International journal of molecular medicine · 2010Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
These experiments were undertaken to assess the importance of cytoplasmic (c) sorbitol oxidation versus mitochondrial (m) pyruvate oxidation in mediating neural and vascular dysfunction attributable to hyperglycemia in diabetic rats. Increased oxidation of sorbitol is coupled to enzymatic reduction of free oxidized NAD(+)c to reduced NADHc, manifested by an increased ratio of NADH to NAD(+)c. Likewise, increased oxidation of pyruvate is coupled to reduction of NAD(+)m to NADHm, which increases the NADH/NAD(+)m ratio. Specific inhibitors of sorbitol production or sorbitol oxidation normalized: increased diabetic nerve NADH/NAD(+)c, impaired nerve-conduction velocity, and vascular dysfunction in sciatic nerve, retina, and aorta; however, they had little or no impact on increased NADH/NAD(+)m. These observations provide, for the first time, strong in vivo evidence for the primacy of sorbitol oxidation versus. pyruvate oxidation in mediating the metabolic imbalances, impaired nerve conduction, and vascular dysfunction evoked by diabetes. These findings are consistent with (a) the fact that oxidation of sorbitol produces "prooxidant" NADHc uncoupled from subsequent production of "antioxidant" pyruvate required for reoxidation of NADHc to NAD(+)c by lactate dehydrogenase, and (b) the hypothesis that neural and vascular dysfunction in early diabetes are caused primarily by increased NADHc, which fuels superoxide production by NADH-driven oxidases.
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Registered trials
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