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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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Bao, X., Wong, V. C. N., Wang, Q., & Low, L. C. K. (1999) · Pediatric Neurology · doi:10.1016/s0887-8994(98)00141-6 · Cited by 37
Diabetic Neuropathy: Pathogenesis and Treatment
Siemionow, M., Külahçı, Y., & Agaoglu, G. (2007) · Elsevier eBooks · doi:10.1016/b978-044452809-4/50165-4 · Cited by 37
Hall, K. E., Sima, A. A. F., & Wiley, J. W. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118530 · Cited by 36
Peripheral neuropathy does not invariably coexist with autonomic neuropathy in diabetes mellitus
Tentolouris, N., Pagoni, S., Τζώνου, Α., & Katsilambros, N. L. (2001) · European Journal of Internal Medicine · doi:10.1016/s0953-6205(00)00128-x · Cited by 36
Amato, A. A., & Dumitru, D. (2002) · Elsevier eBooks · doi:10.1016/b978-1-56053-433-4.50031-6 · Cited by 35
Depletion of myo‐Inositol and Amino Acids in Galactosemic Neuropathy
Nishimura, C., Lou, M. F., & Kinoshita, J. H. (1987) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.1987.tb03428.x · Cited by 34
The pharmacology of diabetic neuropathy
Tomlinson, D. R. (1992) · Diabetes/Metabolism Reviews · doi:10.1002/dmr.5610080107 · Cited by 34
Lambourne, J. E., Brown, A. M., Calcutt, N. A., Tomlinson, D. R., & Willars, G. B. (1988) · Diabetologia · doi:10.1007/bf02341507 · Cited by 34
“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.”
BackgroundMethodResultLi, L., Huang, C., Ai, J., Yan, B., Gu, H., Zhuo-sai, M., Li, A. Y., Xinyan, S., Harden, S. W., Hatcher, J. T., et al. (2010) · The Journal of Comparative Neurology · doi:10.1002/cne.22363 · Cited by 33
“…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
Demerdash, T. M., Seyrek, N. Ç., Smogorzewski, M., Marcinkowski, W., Nasser-Moadelli, S., & Massry, S. G. (1996) · Kidney International · doi:10.1038/ki.1996.526 · Cited by 33
Effects of cilostazol on the peripheral nerve function and structure in STZ-induced diabetic rats
Uehara, K., Sugimoto, K., Wada, R., Yoshikawa, T., Marukawa, K., Yasuda, Y., Kimura, Y., & Yagihashi, S. (1997) · Journal of Diabetes and its Complications · doi:10.1016/s1056-8727(96)00023-2 · Cited by 32
Cation permeability of the blood-brain barrier in streptozotocin-diabetic rats
Jakobsen, J., Knudsen, G. M., & Juhler, M. (1987) · Diabetologia · doi:10.1007/bf00292543 · Cited by 32
“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.”
BackgroundMonosaccharides in Health and Disease
Levine, R. F. (1986) · Annual Review of Nutrition · doi:10.1146/annurev.nu.06.070186.001235 · Cited by 31
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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