The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Impaired rat sciatic nerve sodium-potassium adenosine triphosphatase in acute streptozocin diabetes and its correction by dietary myo-inositol supplementation.
Open accessAbstract
Nerve conduction impairment in experimental diabetes has been empirically but not mechanistically linked to altered nerve myo-inositol metabolism. The phospholipid-dependent membrane-bound sodium-potassium ATPase provides a potential mechanism to relate defects in diabetic peripheral nerve myo-inositol-phospholipid metabolism, impulse conduction, and energy utilization. Therefore, the effect of streptozocin-induced diabetes mellitus and dietary myo-inositol supplementation on rat sciatic nerve sodium-potassium ATPase was studied. ATPase activity was measured enzymatically in sciatic nerve homogenates from 4-wk streptozocin diabetic rats and age-matched controls either fed a standard or 1% myo-inositol supplemented diet. The sodium-potassium ATPase components were assessed by ouabain inhibition or the omission of sodium and potassium ions. Diabetes reduced the composite ATPase activity recovered in crude homogenates of sciatic nerve. The 40% reduction in the sodium-potassium ATPase was selectively prevented by 1% myo-inositol supplementation (which preserved normal nerve conduction). Thus, in diabetic peripheral nerve, abnormal myo-inositol metabolism is associated with abnormal sodium-potassium ATPase activity. The mechanism of the effect of dietary myo-inositol to correct diabetic nerve conduction may be through changes in a sodium-potassium ATPase, possibly via changes in myo-inositol-containing phospholipids.
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“Chronic hyperglycemia enhances formation of advanced glycation end-products (AGEs), which bind to specific receptors (RAGE) and activate inflammatory pathways.”
From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [35]
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“Activation of the polyol pathway further increases oxidative stress, damaging neurons and endothelial cells and reducing blood supply to neural tissues [33–37].”
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Metadata
- Authors
- Greene, D. A., & Lattimer, S. A.
- Affiliations
- University of Pittsburgh (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1983-09-01
- Volume
- 72
- Issue
- 3
- Pages
- 1058-1063
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1129273
- OpenAlex
- W2067323403
- Cited by
- 244
- References
- 31
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 2 · 2017: 1 · 2014: 5 · 2013: 5 · 2012: 3
- FWCI
- 8.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Aldose Reductase and Taurine
- Health Sciences › Medicine › Clinical Neurology › Peripheral Neuropathies and Disorders
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Keywords
- Na+/K+-ATPase, myo-inositol supplementation, streptozotocin-induced diabetes, diabetic peripheral neuropathy, sciatic nerve, nerve conduction, myo-inositol metabolism, dietary supplementation
- MeSH terms
- Acute Disease, Sodium-Potassium-Exchanging ATPase, Animals, Blood Glucose, Body Weight, Diabetes Mellitus, Experimental, Inositol, Male, Nerve Tissue Proteins, Ouabain, Potassium, Rats, Inbred Strains, Sciatic Nerve, Sodium, Rats
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