Myoinositol Uptake by Rat HepatocytesIn Vitro

Chen, Chi-Po; Vu, Van Tien

doi:10.1002/jps.2600680827

Cited by 12 publications

(3 citation statements)

References 21 publications

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“…As an illustration, the depression in neuronal Ins levels and its consequences on phosphoinositide turnover could be the biochemical basis for the effect of lithium on brain function (7)(8)(9)(10). In contrast, the liver, an organ with diverse phosphoinositide species and high rates of metabolic activities, has low micromolar levels of Ins, with no evidence of an energy-and Na ϩ -dependent, high affinity transport system for Ins (11)(12)(13).…”

Section: Myo-inositol (Ins) and Its Polyphosphoinositide Derivatives mentioning

confidence: 99%

Loss of Murine Na+/myo-Inositol Cotransporter Leads to Brain myo-Inositol Depletion and Central Apnea

Berry

Buccafusca

et al. 2003

Journal of Biological Chemistry

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Section: Myo-inositol (Ins) and Its Polyphosphoinositide Derivatives mentioning

confidence: 99%

Loss of Murine Na+/myo-Inositol Cotransporter Leads to Brain myo-Inositol Depletion and Central Apnea

Berry

Buccafusca

et al. 2003

Journal of Biological Chemistry

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“…Similarly, many clinical conditions are associated with hypomagnesemia (i.e., alcoholism and essential hypertension), and diabetic complications are not seen in these situations (11). However, note that not all tissues use an active inositol transport system; e.g., skeletal muscle (25) and liver (26), and these tissues would therefore not be expected to be affected by hypomagnesemia. If there is a direct relationship between inositol depletion and hypomagnesemia, two explanations for the specific tissue distribution of diabetic complications can be proposed.…”

Section: Discussionmentioning

confidence: 99%

Effect of Mg2+ on Na+-Dependent Inositol Transport: Role for Mg2+ in Etiology of Diabetic Complications

et al. 1992

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Diabetes mellitus is associated with a significant reduction in the serum concentration of Mg2+. Several studies have suggested that hypomagnesemia may be implicated in the etiology of diabetic complications; however, no mechanism has been proposed. This study demonstrates that Mg2+ is a positive effector of inositol transport and is capable of promoting a 2.5-fold increase in the affinity of the transporter for inositol. Analysis of the kinetics of inositol transport shows that, at physiological concentrations of inositol, the reductions in Mg2+ concentrations that occur in diabetic patients would result in a significant decline in the rate of inositol transport (1.5- to 2-fold). We suggest that hypomagnesemia may be linked to the development of diabetic complications via reduction in the rate of inositol transport and subsequent intracellular inositol depletion. This assertion allows hypomagnesemia and the polyol theory to be unified into one mechanistic model for the development of diabetic complications.

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“…The various kinetic and biochemical characteristics of SMIT activity among mammalian cell types (2,4,5,8,10,35,38,42,46,61,63,65) and tissues (6,9,14,17,28,(50)(51)(52)(53)59) could imply a more complex gene structure, although small interspecies differences in SGLT1 amino acid sequence are associated with considerable variation in transport kinetics (19). Recently, this laboratory has reexamined the basis for the multiple transcripts ascribed to the human SMIT gene (39,40) in cultured human retinal pigment epithelial (RPE) cells, an in vitro model for diabetic complications (10).…”

mentioning

confidence: 99%

Alternate splicing in human Na⁺-MI cotransporter gene yields differentially regulated transport isoforms

Porcellati¹,

Hosaka²,

Hlaing

et al. 1999

American Journal of Physiology-Cell Physiology

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myo-Inositol is a ubiquitous intracellular organic osmolyte and phosphoinositide precursor maintained at millimolar intracellular concentrations through the action of membrane-associated Na+- myo-inositol cotransporters (SMIT). Functional cloning and expression of a canine SMIT cDNA, which conferred SMIT activity in Xenopus oocytes, predicted a 718-amino acid peptide homologous to the Na+-glucose cotransporter with a potential protein kinase A phosphorylation site and multiple protein kinase C phosphorylation sites. A consistent ∼1.0- to 13.5-kb array of transcripts hybridizing with this cDNA are osmotically induced in a variety of mammalian cells and species, yet SMIT activity appears to vary among different tissues and species. An open reading frame on human chromosome 21 (SLC5A3) homologous to that of the canine cDNA (96.5%) is thought to comprise an intronless human SMIT gene. Recently, this laboratory ascribed multiply sized, osmotically induced SMIT transcripts in human retinal pigment epithelial cells to the alternate utilization of several 3′-untranslated SMIT exons. This article describes an alternate splice donor site within the coding region that extends the open reading frame into the otherwise untranslated 3′ exons, potentially generating novel SMIT isoforms. In these isoforms, the last putative transmembrane domain is replaced with intracellular carboxy termini containing a novel potential protein kinase A phosphorylation site and multiple protein kinase C phosphorylation sites, and this could explain the heterogeneity in the regulation and structure of the SMIT.

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Myoinositol Uptake by Rat HepatocytesIn Vitro

Cited by 12 publications

References 21 publications

Loss of Murine Na+/myo-Inositol Cotransporter Leads to Brain myo-Inositol Depletion and Central Apnea

Loss of Murine Na+/myo-Inositol Cotransporter Leads to Brain myo-Inositol Depletion and Central Apnea

Effect of Mg2+ on Na+-Dependent Inositol Transport: Role for Mg2+ in Etiology of Diabetic Complications

Alternate splicing in human Na⁺-MI cotransporter gene yields differentially regulated transport isoforms

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Myoinositol Uptake by Rat HepatocytesIn Vitro

Cited by 12 publications

References 21 publications

Loss of Murine Na+/myo-Inositol Cotransporter Leads to Brain myo-Inositol Depletion and Central Apnea

Loss of Murine Na+/myo-Inositol Cotransporter Leads to Brain myo-Inositol Depletion and Central Apnea

Effect of Mg2+ on Na+-Dependent Inositol Transport: Role for Mg2+ in Etiology of Diabetic Complications

Alternate splicing in human Na+-MI cotransporter gene yields differentially regulated transport isoforms

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Alternate splicing in human Na⁺-MI cotransporter gene yields differentially regulated transport isoforms