Inositol Uptake Research Articles

Inositol uptake by cultured isolated rat Schwann cells

The uptake of radiolabeled myo-inositol by Schwann cells isolated from the sciatic nerve of 2–4 day old rats was found to occur by a saturable, sodium-dependent phlorizin-inhibited mechanism with an estimated K m of 30μM. The system was inhibited by galactose and glucose but not by galactitol. At high concentrations of myo-inositol, a diffusion-like process appeared to be functional. The characteristics of the saturable system are very similar to those of myo-inositol uptake by the endoneural fascicle preparation of sciatic nerve.

The Effect of Cyproterone Acetate on Myo‐Inositol Uptake and Secretion in the Reproductive Tract of the Male Rat

A procedure is described for evaluating the uptake of myo‐inositol by measuring the radioactivity (dpm/mg wet weight of tissue) in the male reproductive accessory glands after injection of (2‐3H)myo‐inositol into bilaterally nephrectomized rats. The rate of secretion of the labelled inositol was assessed by measuring the total dpm in fluids expressed from the seminal vesicles and coagulating glands after injection of the tritiated inositol.Cyproterone acetate treatment (15 mg/day), for 2 to 7 days, inhibited secretion of radioactive inositol by the seminal vesicles and decreased the uptake capacity to a greater extent than it inhibited the rate of inositol accumulation into these glands. It had a similar effect on the coagulating glands after 7 days of treatment. The prostate was the least affected by the cyproterone acetate treatment.

On the uptake of inositol by rat brain synaptosomes.

AbstractThe uptake of inositol by rat brain synaptosomes occurs via an unsaturable process that even at substrate concentrations as low as 1 μM is unable to achieve a concentration gradient indicative of active transport. Dinitrophenol, ouabain and cytochalasin B did not affect uptake of the cyclitol. The data indicate that inositol uptake by rat synaptosomes occurs by diffusion or by a system with an affinity so low it is difficult to discern. The low capacity, saturable inositol uptake system observed in rabbit brain slices may reflect a species difference or uptake by elements of the slice other than neuronal membranes.

Phospholipid effects on the rat lens transport systems

The in vitro effects of phosphatidyl choline, phosphatidyl ethanolamine, phosphatidyl serine, sphingomyelin, lysophosphatidyl choline, lysophosphatidyl ethanolamine, lysophosphatidyl serine, glycerophosphoryl choline, and phosphatidic acid on rubidium uptake and amino acid transport of rat lens are presented. None of these lipids affected the rubidium uptake mechanism; however, a large increase in the apparent leak-out of rubidium was observed with lysophosphatidyl choline. Lysophosphatidyl choline also inhibited all of the amino acid transport systems (A, ASC, L, Gly, Ly and β) as well as the uptake of inositol.

The uptake of vitamins by mouse fibroblast cells (strain LS) during growth in a chemically defined medium

ABSTRACT The uptake of biotin, choline, folic acid, hypoxanthine, inositol, nicotinamide, pantothenic acid, pyridoxine, riboflavin, thiamine and vitamin B12 by mouse LS cells in suspension culture was determined by microbiological assay methods. Based on the extent of uptake during cell growth, vitamin growth yields (cells produced/unit mass of vitamin utilized) were estimated for all of the vitamins, except folic acid, thiamine and B12. The growth yields were lower during the early phases of culture. No uptakes of folic acid or B12 could be demonstrated. During the period of incubation about half of the thiamine was irretrievably lost through spontaneous decomposition.

Inositol production by the brain in normal and alloxan-diabetic dogs

It was found that there was no net uptake of inositol by CSF from plasma, indicating that the high concentration of inositol in the CSF relative to that in plasma of normal and diabetic dogs originates from inositol synthesized by brain. The inositol concentration and rate of efflux from the CSF were used to measure inositol turnover in CSF, and from this was calculated a minimum rate of inositol production by dog brain in vivo. There was no significant difference in the rate of inositol production by the brain (88 μmoles/kg brain/h) between the normal and alloxan-diabetic dog.

Myo-inositol transport in slices of rat kidney cortex : I. Effect of incubation conditions and inhibitors

The incubation conditions affecting the energy- and sodium ion-requiring uptake and retention of myo-inositol by slices of rat kidney cortex have been studied. No transport could be demonstrated in other tissues. Leakage of inositol from the slices amounted to 15% of the endogenous inositol in the first 45 min of incubation in air and at most to 8% on reincubation for 1 h in 95% O 2-5% CO 2. Removal of oxygen from the gas phase increased leakage and abolished the active uptake of inositol, effects which could not be prevented by the addition of energy sources such as glucose and ATP. The accumulation of radioactivity had a Q 10 greater than 3 and an apparent K m of 1.57·10 −4 M. A number of inhibitors of different stages of metabolic energy production interfered in varying degree with the uptake and retention of inositol. The extent of inhibition was largely determined by the concentration of the substance used, but an anomalous response was seen with 2,4-dinitrophenol. The results are discussed with reference to current concepts of active transport.

Myo-inositol transport in slices of rat kidney cortex : II. Effect of the ionic composition of the medium

The effect of changes in the ionic composition of the incubation medium on the active uptake and retention of myo-inositol by cortex slices from rat kidneys has been assessed. The Na + requirement could not be satisfied by Li +, K +, Rb +, Cs +, choline + or Tris +. K + (>4 mM) was necessary for optimal uptake and retention of inositol, but could be replaced completely with Rb +, Cs + was only partly effetive in place of K +, whereas Li + and NH 4 + were ineffective. The effects on inositol uptake and leakage produced by the substitution of choline + for Na + were largely reversible, indicating that choline had not permanently damaged the slices. Neither glucose nor ATP restored the values of the two parameters examined to normal in the absence of K + or at low levels of Na +. Na + alone was not able to maintain the integrity of the system. Both Ca 2+ and Mg 2+ at optimal concentrations of 1 mM and 1–2 mM, respectively, were required, but could be replaced by Sr 2+ concentrations as low as 0.75 mM. The inhibition of inositol uptake by ouabain in Krebs-Ringer bicarbonate media also occurred, when K + was either omitted or replaced by other monovalent cations. It was partly prevented by increased concentrations of K +, Cs + or, especially, Rb +, but not by Ca 2+. The effects of cations are discussed in terms of the mechanism of active transport of non-electrolytes and cations and of the integrity of renal tubular membranes.

Localization of phospholipase A 2 in outer membrane of mitochondria

We examined the effect of etomoxir treatment on de novo cardiolipin (CL) biosynthesis in H9c2 cardiac myoblast cells. Etomoxir treatment did not affect the activities of the CL biosynthetic and remodeling enzymes but caused a reduction in [1-14C]palmitic acid or [1-14C]oleic acid incorporation into CL. The mechanism was a decrease in fatty acid flux through the de novo pathway of CL biosynthesis via a redirection of lipid synthesis toward 1,2-diacyl-sn-glycerol utilizing reactions mediated by a 35% increase (P < 0.05) in membrane phosphatidate phosphohydrolase activity. In contrast, etomoxir treatment increased [1,3-3H]glycerol incorporation into CL. The mechanism was a 33% increase (P < 0.05) in glycerol kinase activity, which produced an increased glycerol flux through the de novo pathway of CL biosynthesis. Etomoxir treatment inhibited 1,2-diacyl-sn-glycerol acyltransferase activity by 81% (P < 0.05), thereby channeling both glycerol and fatty acid away from 1,2,3-triacyl-sn-glycerol utilization toward phosphatidylcholine and phosphatidylethanolamine biosynthesis. In contrast, etomoxir inhibited myo-[3H]inositol incorporation into phosphatidylinositol and the mechanism was an inhibition in inositol uptake. Etomoxir did not affect [3H]serine uptake but resulted in an increased formation of phosphatidylethanolamine derived from phosphatidylserine.The results indicate that etomoxir treatment has diverse effects on de novo glycerolipid biosynthesis from various metabolic precursors. In addition, etomoxir mediates a distinct and differential metabolic channeling of glycerol and fatty acid precursors into CL.

Energy- and sodium-dependent uptake of inositol by kidney cortex slices

Energy- and sodium-dependent uptake of inositol by kidney cortex slices

A study of the role of inosito in the nutrition of Nematospora gossypii and Saccharomyces carlsbergensis.

SUMMARY: A study has been made of the uptake of inositol from liquid media by Nematospora gossypii and Saccharomyces carlsbergensis 4228. All the available inositol was rapidly removed from the medium so long as growth continued. Small amounts were recovered from the organisms by water extraction, and up to 75% from the yeast by acid hydrolysis. This bound inositol in the yeast possessed properties resembling those of phytin. On media deficient in inositol, cell division was incomplete. No influence of inositol on the respiratory system of S. carlsbergensis could be detected. γ-Hexachlorocyclohexane inhibited growth and respiration of intact yeast cells, but not respiration of dried yeast preparations; its effect was not reversed by inositol. Streptidine, strepturea and streptamine neither inhibited growth nor could replace inositol as a growth factor.