Measurement of myo-inositol in single cells and defined areas of the nervous system by selected ion monitoring

Sherman, William R.; Packman, Paul M.; Laird, Michael H.; Boshans, Rita L.

doi:10.1016/0003-2697(77)90015-x

Cited by 44 publications

(24 citation statements)

References 11 publications

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“…Our data therefore provide no new support for the role of sorbitol and fructose in the genesis of diabetic neuropathy. Our results do demonstrate, however, that both aldose reductase and sorbitol dehydrogenase (sorbitol + fructose) are active in human nerve and can bring about elevations in the levels of sorbitol and fructose in human diabetes as well as that in the rat [25]. Whether or not this leads to abnormalities remains unknown.…”

Section: Discussioncontrasting

confidence: 71%

Human diabetic endoneurial sorbitol, fructose, and myo‐inositol related to sural nerve morphometry

Dyck¹,

Sherman²,

Hallcher³

et al. 1980

Annals of Neurology

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498

270

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Fascicles of the sural nerve from each of 20 diabetic patients, mostly with maturity-onset diabetes, were studied by biochemical and pathological techniques, and results were compared to values found in nerve specimens from 15 healthy persons. The sorbitol and fructose content was much more variable in diabetic than in healthy nerves. More than one-third of the diabetic nerves had sorbitol and fructose values above the highest levels for controls. myo-Inositol and scyllo-inositol content was not reduced in diabetic nerves. The sorbitol, fructose, and inositol concentrations could not be related to clinical, neurophysiological, or pathological severity of neuropathy. A comparison of scored symptoms and signs and clinical neurophysiological studies against morphometric and teased fiber studies of sural nerve demonstrated that the former three provide sensitive and reliable measures of severity of neuropathy that can be used for controlled clinical trials of diabetic neuropathy. The presence and type of teased fiber abnormalities could be related to the duration of diabetes and to symptoms of neuropathy. In untreated diabetics without symptoms of neuropathy, a higher than normal frequency of teased fibers showing segmental demyelination and remyelination was found. Untreated diabetics with symptomatic neuropathy showed two kinds of abnormalities: fibers with segmental demyelination and remyelination and fibers undergoing axonal degeneration. In treated diabetics, who often had longstanding neuropathy, the most common abnormalities were fibers undergoing axonal degeneration.

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Section: Discussioncontrasting

confidence: 71%

Human diabetic endoneurial sorbitol, fructose, and myo‐inositol related to sural nerve morphometry

Dyck¹,

Sherman²,

Hallcher³

et al. 1980

Annals of Neurology

Self Cite

498

270

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show abstract

“…A study on myoinositol content of individual brain cells in vivo revealed that the exceptionally high myoinositol, present in central nervous system, was not a feature of all cells (16). A similar phenomenon could occur in other organs, especially in the lung with its more than 40 different cells.…”

Section: Discussionmentioning

confidence: 95%

“…The enhanced myoinositol turnover, as an early postreceptor event involves hydrolysis of phosphoinositide (resulting in a change in membrane characteristics) and a subsequent incorporation into phosphoinositide. However, the concentration of myoinositol in individual cells may not be uniform (16) and a given myoinositol pool within the tissue may not be associated with postreceptor events involving enhanced turnover (17).…”

mentioning

confidence: 99%

Perinatal Development of Myoinositol Uptake into Lung Cells: Surfactant Phosphatidylglycerol and Phosphatidylinositol Synthesis in the Rabbit

et al. 1986

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ABSTRACT. It has been proposed that the high serum myoinositol promotes fetal growth and affects development of lung surfactant. However, it is unclear how the extracellular myoinositol becomes available in specific cells and whether &ere are developmental differences in myoinositol uptake. In the present study the mechanisms and perinatai development of intracellular myoinositol uptake into rabbit lung cells were investigated. Lung slices, lung explants, and type I1 alveolar cells were used. Evidence of saturable, sodium-and energy-dependent, and of non-saturable, sodium-and energy-independent myoinositol uptake was found. The nonsaturable uptake decreased by 67% during spontaneous maturation, as studied in lung slices. Betamethasone (0.2 mg/kg days 26.3 and 27.3, to the doe) decreased by 65% the nonsaturable myoinositol uptake in 28-day-old fetuses. However, the saturable uptake revealed only small changes during perinatal development. The effect of extracellular myoinositol on surfactant phospholipid synthesis was evaluated in lung explants from 28-day-old fetuses, cultured for 2 days. In the presence of M dexamethasone the concentration of extracellular myoinositol, required for half-maximal inhibition of surfactant phosphatidylglycerol incorporation was higher than in explants grown without the hormone (approximately 0.4 versus 0.2 mM). However, in the microsomal fraction the phosphatidylglycerol incorporation was always inhibited by as low as 4 pM myoinositol. Myoinositol was taken up by isolated type I1 cells preferably by nonsaturable mechanism. The -ihosphatidylglycerol incorporation was less sensitive to extracellular mvoinositol in adult than in fetal cells. Although there were bnly small changes in the concentration of free myoinositol in whole lung during perinatal development, the availability of this sugar alcohol to some specific cells decreased strikingly due to a decrease in serum concentration and a decrease in permeability of this putative growth factor. The present findings demonstrate that some cells within myoinositol-rich tissue can be devoid of this sugar alcohol and critically depend on extracellular source for their myoinositol supply. (Pediatr Res 20: 179-185, 1986)

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“…Free myo-inositol is highly and selectively concentrated within specific cell populations in brain, and a similarly heterogeneous distribution may occur in peripheral nerve (49). Since the high tissue level of myo-inositol in peripheral nerve has been variously attributed by indirect means to both the axon (50) and the Schwann cell (38), cellular localization of sodium-dependent myo-inositol uptake within peripheral nerve remains controversial.…”

Section: Methodsmentioning

confidence: 99%

Sodium- and energy-dependent uptake of myo-inositol by rabbit peripheral nerve. Competitive inhibition by glucose and lack of an insulin effect.

Greene¹,

Lattimer²

1982

J. Clin. Invest.

147

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A B S T R A C T Experimental diabetes consistently reduces the concentration of free myo-inositol in peripheral nerve, which usually exceeds that of plasma by 90-100-fold. This phenomenon has been explicitly linked to the impairment of nerve conduction in the acutely diabetic streptozocin-treated rat. However, the mechanism by which acute experimental diabetes lowers nerve myo-inositol content and presumably alters nerve myo-inositol metabolism is unknown. Therefore, the effects of insulin and elevated medium glucose concentration on 2-[3H]myo-inositol uptake were studied in a metabolically-defined in vitro peripheral nerve tissue preparation derived from rabbit sciatic nerve, whose free myo-inositol content is reduced by experimental diabetes. The results demonstrate that myo-inositol uptake occurs by at least two distinct transport systems in the normal endoneurial preparation. A sodium-and energy-dependent saturable transport system is responsible for at least 94% of the measured uptake at medium myo-inositol concentrations approximating that present in plasma. This carrier-mediated transport system has a high affinity for myo-inositol (K, = 63 gtM), and is not influenced acutely by physiological concentrations of insulin; it is, however, inhibited by hyperglycemic concentrations of glucose added to the incubation medium in a primarily competitive fashion. Thus, competitive inhibition of peripheral nerve myo-inositol uptake by glucose may constitute a mechanism by which diabetes produces physiologically significant alterations in peripheral nerve myo-inositol metabolism.

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Measurement of myo-inositol in single cells and defined areas of the nervous system by selected ion monitoring

Cited by 44 publications

References 11 publications

Human diabetic endoneurial sorbitol, fructose, and myo‐inositol related to sural nerve morphometry

Human diabetic endoneurial sorbitol, fructose, and myo‐inositol related to sural nerve morphometry

Perinatal Development of Myoinositol Uptake into Lung Cells: Surfactant Phosphatidylglycerol and Phosphatidylinositol Synthesis in the Rabbit

Sodium- and energy-dependent uptake of myo-inositol by rabbit peripheral nerve. Competitive inhibition by glucose and lack of an insulin effect.

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