Cited by 244Aldose Reductase and TaurinePeripheral Neuropathies and DisordersPain Mechanisms and Treatments

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Impaired rat sciatic nerve sodium-potassium adenosine triphosphatase in acute streptozocin diabetes and its correction by dietary myo-inositol supplementation.

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Greene, D A, Lattimer, S A·1983·Journal of Clinical Investigation

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Abstract

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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Lin, M., Harden, S. W., Li, L., Wurster, R. D., & Cheng, Z. J. (2009) · Autonomic Neuroscience · doi:10.1016/j.autneu.2009.09.020 · Cited by 10
“3) 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 et al., 1975; Greene and Lattimer, 1983; Inada et al., 2008, Shoham et al., 2003).”
BackgroundResult
Reduced adenosine triphosphatase activity and motor nerve conduction velocity in l-fucose-fed rats is reversible after dietary normalization
Yorek, M. A., Wiese, T. J., Davidson, E. P., Dunlap, J. A., & Conner, C. E. (1996) · Metabolism · doi:10.1016/s0026-0495(96)90059-1 · Cited by 10
An aldose reductase inhibitor but not myo-inositol blocks enhanced polyphosphoinositide turnover in peripheral nerve from diabetic rats
Berti‐Mattera, L. N., Day, N. S., Peterson, R. G., & Eichberg, J. (1996) · Metabolism · doi:10.1016/s0026-0495(96)90285-1 · Cited by 10
Inability of insulin to maintain normal nerve function during high‐frequency stimulation in diabetic rat tail nerves
Andersen, H., Nielsen, J. F., & Nielsen, V. K. (1994) · Muscle & Nerve · doi:10.1002/mus.880170111 · Cited by 10
Clinical trials of sorbinil on nerve function
Pfeifer, M. A. (1986) · Metabolism · doi:10.1016/0026-0495(86)90192-7 · Cited by 10
Insulin resistance, a result of reduced synthesis of prostaglandylinositol cyclic phosphate, a mediator of insulin action?
Wasner, H. K., Salge, U., Psarakis, E., & Niktopoulos, A. (1997) · Acta Diabetologica · doi:10.1007/s005920050085 · Cited by 11
THE EFFECTS OF ORAL ADMINISTRATION OF DIFFERENT DOSES OF HYDROALCOHOLIC EXTRACT OF SILYMARIN ON STATUS OF SERUM TRACE ELEMENTS
Sajedianfard, J., Nazıfı, S., & Shamsaei, H. A. (2014) · American Journal of Animal and Veterinary Sciences · doi:10.3844/ajavsp.2014.170.176 · Cited by 9
Effect of myo-inositol on renal Na-K-ATPase in experimental diabetes
Cohen, R. A., MacGregor, L. C., Spokes, K., Silva, P., & Epstein, F. H. (1990) · Metabolism · doi:10.1016/0026-0495(90)90161-5 · Cited by 9
Sodium, Potassium-Activated Adenosine Triphosphatase Activity Is Impaired in the Guinea Pig Pancreatic Duct System in Streptozotocin-Induced Diabetes
Hootman, S. R., Jones, J. E., Kapoor, R., Nguyen, K.-L., & de Ondarza, J. (1998) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1998.8195 · Cited by 9
Binding of an aldose reductase inhibitor to renal glomeruli
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Altered Nerve Myo-Inositol Metabolism in Experimental Diabetes and Its Relationship to Nerve Function
Greene, D. A., & Lattimer, S. A. (1985) · Humana Press eBooks · doi:10.1007/978-1-4612-5184-2_37 · Cited by 9
Self-citation
Effect of diabetes and Sorbinil treatment on phospholipid metabolism in rat glomeruli
Cohen, M. P., Klepser, H., & Cua, E. (1986) · Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism · doi:10.1016/0005-2760(86)90278-x · Cited by 8
2-Chloroadenosine reverses hyperglycemia-induced inhibition of phosphoinositide synthesis in cultured human retinal pigment epithelial cells and prevents reduced nerve conduction velocity in diabetic rats
Kato, K., Thomas, T. P., Stevens, M. J., Greene, D. A., & Nakamura, J. (1999) · Metabolism · doi:10.1016/s0026-0495(99)90213-5 · Cited by 8
Self-citation
Reduced capability of transmitting high frequency impulses in tail nerves of diabetic rats
Nielsen, J. F., Andersen, H., & Nielsen, V. K. (1993) · Muscle & Nerve · doi:10.1002/mus.880160307 · Cited by 7
A combination of the aldose reductase inhibitor, statil, and the prostaglandin E1 analogue, OP1206.αCD, completely improves sciatic motor nerve conduction velocity in streptozocin-induced chronically diabetic rats
Yasuda, H., Sonobe, M., Hisanaga, T., Kawabata, T., Maeda, K., Kikkawa, R., & Shigeta, Y. (1992) · Metabolism · doi:10.1016/0026-0495(92)90320-a · Cited by 7
Effect of Sorbinil and Ascorbic Acid on myo‐Inositol Transport in Cultured Rat Schwann Cells Exposed to Elevated Extracellular Glucose
Karihaloo, A. K., Joshi, K., & Chopra, J. S. (1997) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1997.69052011.x · Cited by 7
Rapid actions of insulin on sensory nerve function
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Nerve Microvessel Changes in Diabetes are Prevented by Aldose Reductase Inhibition
Benstead, T. J., & SANGALANG, V. E. (1995) · Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques · doi:10.1017/s0317167100039834 · Cited by 7
Vascular factors in the causation of diabetic neuropathy
Thomas, P. K. (1987) · Trends in Neurosciences · doi:10.1016/0166-2236(87)90114-7 · Cited by 7
Phosphoinositides provide a regulatory mechanism of surface charge and active transport
Cerbón, J., Ontiveros, C., & Janovitz, A. (1986) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/0167-4889(86)90155-2 · Cited by 7
The Polyol Pathway in Dysfunction of Diabetic Peripheral Nerve
Greene, D. A., & Lattimer, S. A. (1985) · Diabetic Medicine · doi:10.1111/j.1464-5491.1985.tb00638.x · Cited by 7
Self-citation
Chronic insulinopenia/hyperglycemia decreases cannabinoid CB1 receptor density and impairs glucose uptake in the mouse forebrain
Moura, L. I. F., Lemos, C., Ledent, C. A., Carvalho, E., & Köfalvi, A. (2019) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2019.01.024 · Cited by 6
“It has been shown before that the activity of Na+/K+-ATPases is decreased in both the peripheral nerves (Greene and Lattimer 1983; Catanzaro et al. 2013) and in the blood-brain barrier (Jakobsen et al.”
Background
Elevated Levels of Glucose and L‐Fucose Reduce 22Na+ Uptake and Whole Cell Na+ Current in Cultured Neuroblastoma Cells
Yorek, M. A., Stefani, M. R., & Wachtel, R. E. (1994) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1994.62010063.x · Cited by 6
Erythrocytes from diabetics with neuropathy have fewer sodium pumps
Noda, K., Umeda, F., Hashimoto, T., Yamashita, T., & Nawata, H. (1990) · Diabetes Research and Clinical Practice · doi:10.1016/0168-8227(90)90114-9 · Cited by 6
Myocardial inositol and sodium in diabetes
Regan, T. J., Beyer-Mears, A., Torres, R., & Fusilli, L. D. (1992) · International Journal of Cardiology · doi:10.1016/0167-5273(92)90260-a · Cited by 6
Are mitogen-activated protein kinases glucose transducers for diabetic neuropathies?
Purves-Tyson, T. D., & Tomlinson, D. R. (2002) · International review of neurobiology · doi:10.1016/s0074-7742(02)50074-x · Cited by 6

Authors: Greene, D. A., & Lattimer, S. A.
Affiliations: University of Pittsburgh (US)
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1983-09-01
Volume: 72
Issue: 3
Pages: 1058-1063
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci111030
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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Impaired rat sciatic nerve sodium-potassium adenosine triphosphatase in acute streptozocin diabetes and its correction by dietary myo-inositol supplementation.

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