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.
“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]
The Introduction and the section “Effect of streptozocin diabetes and dietary MI” discuss hyperglycemia in relation to myo-inositol uptake, polyol-pathway activity, and nerve sodium-potassium ATPase. Searches for advanced glycation end-products, RAGE, and inflammatory pathways found no passage addressing the claimed mechanism in our copy; page numbers were not provided. (LLM, conf=0.77)
Experimental — accuracy not yet measuredActivation of the polyol pathway further increases oxidative stress, damaging neurons and endothelial cells and reducing blood supply to neural tissues.
“Activation of the polyol pathway further increases oxidative stress, damaging neurons and endothelial cells and reducing blood supply to neural tissues [33–37].”
From Diabetic gastroparesis: pathophysiology and impact on insulin timing choices (2026) · cites this paper as [35]
The Introduction and the section on streptozocin diabetes and dietary myo-inositol suggest that increased polyol-pathway activity may lower nerve myo-inositol and impair nerve function. Our copy does not address the claimed oxidative-stress mechanism, damage to endothelial cells, or reduced blood supply to neural tissue (searched: oxidative stress, endothelial cells, vascular blood flow). (LLM, conf=0.73)
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“Aliquots of homogenate were assayed enzymatically for total and ouabain-insensitive ATPase activity as described (45).”
MethodSelf-citationExperimental diabetes mellitus impairs the function of the retinal pigmented epithelium
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“Hexokinase directs glucose into the glycolytic pathway under normoglycemic conditions, however, there is a glucose concentration-dependent activation of aldose reductase in nerve (Greene and Lattimer, 1983; Greene et al., 1984; 1987).”
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“The reduction in ouabain-sensitive ATPase activity in the nerves of our diabetic rats was of similar magnitude to that reported by others, but it took longer to develop; Greene and Lattimer [11] claim full reduction of activity after within 4 weeks of induction of streptozotocin-induced diabetes.”
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“…with STZ-induced diabetic animal models due to the fact that STZ is carcinogenic and may have direct toxic effects on multiple organs including the heart, kidney, and liver, as well as the nervous system (Greene and Lattimer, 1983; Shoham et al., 2003; Wold and Ren, 2004; Inada et al., 2008).”
BackgroundPathways through which glucose induces a rise in [Ca2+]i of polymorphonuclear leukocytes of rats
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“Experimental diabetes seems to initiate a defect in Na+/K+-pump activity in peripheral nerves [13, 14] and in skeletal and heart muscle [15] of streptozotocin-diabetic as well as in spontaneously diabetic rats.”
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- 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 › Neurology › Peripheral Neuropathies and Disorders
- Health Sciences › Medicine › Physiology › 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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