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Significant rise of fructose in the blood plasma of cattle resulted from an application of sorbite solution (0.5 g sorbite per kg live weight), with its onset as early as during the infusion. The highest concentration was reached 15 minutes after completion of infusion. Rise in glucose (11 mg/100 ml plasma on average) failed to prove statistically significant and dropped temporarily (after 60 to 120 minutes) below the original value. The lactate level in the blood went up temporarily and reached its maximum 30 minutes from the end of infusion. Sorbite solution (1 g/kg live weight) was intravenously applied to sheep and tock fructose to its maximum after 30 minutes. Intraperitoneal application of sorbite solution (1 g/kg live weight) was tolerated well also by piglets and triggered an age-dependent decline of glucose in blood plasma.
Sorbitol metabolism was examined with a sorbitol-fermenting strain (160) of Streptococcus sanguis isolated from the dental plaque of a subject using sorbitol-containing chewing-gum for 4 years. S. sanguis 160 was grown in continuous culture (pH, 7.0; dilution rate, 0.1 h-1) with glucose, sorbitol and nitrogen (sorbitol-excess) limitations. Cells grown with a glucose limitation exhibited low, but detectable, uptake of [14C]-sorbitol and transition to medium limiting in sorbitol resulted in a 5-fold increase in sorbitol uptake. Kinetic data revealed that both glucose and sorbitol-limited cells possessed 2 transport systems for sorbitol (Ks = 3.3-6.7 and 36-64 microM), but continued growth of the organism on limiting sorbitol resulted in the loss of the high-affinity system. Decryptified, sorbitol-limited cells phosphorylated sorbitol in the presence of phosphoenolpyruvate (PEP), but not with ATP, indicating sorbitol transport solely via the PEP phosphotransferase (PTS) system. PEP-dependent activity in glucose-limited and sorbitol-excess cells was 6- and 4-fold lower than that of the sorbitol-limited cells. Uptake of [14C]-sorbitol and activity for Ell for sorbitol [Ellsor] of the PTS in cells in transition from a glucose to sorbitol limitation confirmed the induction of the sorbitol-PTS and the repression of the glucose-PTS in the presence of sorbitol. Cells grown with an excess of sorbitol exhibited very low Ellsor activity. A crossover experiment with membranes and soluble fractions from glucose-, sorbitol- and nitrogen-limited cells of S. sanguis 160 demonstrated the induction of a soluble PTS component in sorbitol-limited cells essential for sorbitol transport via the PTS.(ABSTRACT TRUNCATED AT 250 WORDS)
Sorbitol transport by oral streptococci was mediated by a phosphoenolpyruvate phosphotransferase system (PTS). The transition of S. sanguis 160 from continuous growth on limiting glucose to limiting sorbitol resulted in induction of EIIsor of the sorbitol-PTS, as well as sorbitol-6-P dehydrogenase which converts sorbitol-6-P to fructose-6-P. Sorbitol transport activity required the presence of a soluble sorbitol-specific component of the PTS, tentatively identified as an enzyme III for sorbitol (IIIsor). In addition, the results indicated that sorbitol transport can be mediated by the ELLglc, particularly in the presence of the sorbitol-specific component. S. sanguis 160 utilized sorbitol in a manner different from that reported for S mutans. Growth on glucose by S. sanguis 160 was inhibited by the presence of sorbitol in the growth medium and sorbitol was utilized in the presence of glucose. In addition, pulses of glucose added to cultures growing on sorbitol resulted in expulsion of sorbitol from the cell. Sorbitol was shown to interfere with glucose metabolism by S. sanguis 160 by inhibiting glucose transport by sorbitol-limited cells, but not by glucose-limited cells, and by inhibiting glycolytic activity with glucose as the substrate. Furthermore, sorbitol was an effective repressor of the glucose-PTS, exhibiting negative regulation over synthesis of both EIIglc and a soluble component of the glucose-PTS, presumably IIIglc. Oral streptococci metabolize sorbitol to large amounts of formate and ethanol in addition to smaller amounts of lactate and acetate. The metabolism of sorbitol by S. sanguis and S. gordonii was less sensitive to oxygen than that by S. mutans and S. mitis.
BACKGROUND: Sorbitol plays an important role in renal osmoregulation. In the rat renal inner medulla sorbitol synthesis and sorbitol degradation are located in different cell types. Whereas sorbitol synthesis can be detected in the inner medullary collecting duct cells, sorbitol degradation takes place in the interstitial cells. Therefore, one can speculate that the cooperation between epithelial and interstitial cells requires sorbitol transport into interstitial cells. METHODS: Our studies were performed with an interstitial cell line derived from the renal inner medulla of Wistar rats. These cells have typical characteristics of renal fibroblasts. In addition, they possess a high activity of sorbitol dehydrogenase as determined in vivo. Uptake was measured by liquid scintillation counting. For studies on sorbitol metabolism sorbitol concentration was measured photometrically. RESULTS: The results show that sorbitol transport into interstitial cells occurs via a yet to be described transport system. No saturation of sorbitol transport could be found up to an extracellular sorbitol concentration of 80 mmol/L. The transport was neither sodium nor chloride dependent. Trans-stimulation increased the sorbitol uptake. Sorbitol uptake was less inhibited by cytochalasin B than 2-deoxy-D-glucose uptake. The transport showed a high affinity for sorbitol and only little inhibition of sorbitol uptake by substances with a similar structure was observed. CONCLUSIONS: Our results show a new sorbitol transport system in renal inner medullary interstitial cells, which is rather different from the described sorbitol permease in renal epithelial cells and from glucose transporters of the GLUT- and SGLT-family.
The renal papillary epithelial cell line, GRB-PAP1, accumulates sorbitol when grown in a hypertonic (500 mosmol/kgH2O) bathing medium. When the cells are returned to a 300 mosmol/kgH2O medium, they lose their sorbitol rapidly to the bath. Sorbitol movement across the membranes of these cells was investigated by studying the uptake of radioactive sorbitol and related compounds. Sorbitol uptake increased 71-fold when cells grown in 500 mosmol/kgH2O medium were exposed to a 300 mosmol/kgH2O test solution. The magnitude of the permeability increase was proportional to the size of the change in the osmolality of the bathing medium and not the absolute osmolality. Sorbitol uptake was a linear function of medium sorbitol concentration with no sign of saturation at sorbitol concentrations up to 315 mM. Although the permeability of other polyols was increased when the osmolality was reduced, competition between sorbitol and related sugars and polyols could not be demonstrated. Both the increased sorbitol uptake after a decrease in medium osmolality and the decrease to control permeability after return to the original osmolality were complete within 30 s. A wide variety of transport inhibitors and ion substitutions failed to alter the magnitude of the sorbitol permeability increase. The most effective inhibitor was quinidine, 1 mM reducing sorbitol uptake by 73%. The sorbitol permeability increase could also be blocked by reducing the temperature to 0 degrees C. Nonspecific uptake of sorbitol, such as endocytosis, was shown to be of only minor significance. The large increase in sorbitol permeability and subsequent sorbitol efflux enables these cells to withstand large decreases in osmolality without excessive swelling and consequent damage. A similar compensatory mechanism may operate in vivo in the renal papilla during the onset of diuresis.
The aim of our study was to test the hypothesis that the better absorption of sorbitol when ingested with glucose could be related to a delayed gastric emptying. We tested the effect of the ingestion of glucose and lipids on the gastric emptying and intestinal absorption of sorbitol in six healthy volunteers, using gastric scintigraphy and hydrogen breath test. After an overnight fast, subjects ingested in random order, on 48-h test periods separated by at least one week, the following solutions: (a) 20 g sorbitol alone; (b) 20 g sorbitol and 20 g glucose; (c) 20 g sorbitol and 9 g lipids. Isotopic acquisitions were taken for 3 h following the ingestion of sorbitol labelled with 111Indium. Hydrogen concentration was measured in end-expiratory samples during 5 h, and the areas under the breath hydrogen curve, reflecting the amounts of sorbitol unabsorbed in the small bowel, were compared between periods. Mean area under the curve was 397 +/- 159 when sorbitol was ingested alone, and this was significantly lower when ingested with glucose or lipids (313 +/- 181 and 337 +/- 135, respectively; P < 0.05). The three curves of sorbitol gastric emptying differed significantly from each other, the gastric emptying being the slowest for sorbitol plus lipids, and the fastest for sorbitol taken alone. We found a positive correlation between the half-emptying time and the hydrogen areas under the curve (r = 0.46, P = 0.05). In conclusion, our study demonstrates that adding glucose or lipids to a solution of sorbitol slows the gastric emptying of sorbitol, resulting in a better intestinal absorption of sorbitol.
Clinical studies in Sweden have shown that the proportion of sorbitol-utilizing strains of Streptococcus sanguis increases in dental plaque from individuals using sorbitol-containing products for prolonged periods. We have undertaken to study the metabolism of glucose and sorbitol by S. sanguis 160, isolated from a subject consuming sorbitol-containing chewing-gum 4 times a day for 4 years. Growth on glucose was inhibited by the presence of sorbitol in the growth medium and sorbitol was utilized in the presence of glucose, albeit, at a slower rate than glucose. In addition, pulses of glucose added to cultures growing on sorbitol resulted in the expulsion of sorbitol from the cell. In order to examine further the relationship of sorbitol and glucose, uptake assays were carried out with S. sanguis 160 grown in continuous culture (pH 7.0, dilution rate = 0.1 h-1) with glucose, sorbitol or nitrogen (sorbitol excess) limitations. The uptake of [14C]-glucose by sorbitol-limited cells, but not by glucose-limited cells, was inhibited by sorbitol, as was glycolysis. Kinetic experiments with glucose-limited cells showed 2 transport systems for glucose with Ks values of 5.2 and 40 microM, and glucose phosphorylation activity by decryptified cells indicated transport by the P-enolpyruvate (PEP) phosphotransferase system (PTS) with lesser activity for an ATP-dependent transport process. Transition from glucose-limited growth to sorbitol-limited growth revealed repression of total [14C]-glucose uptake by intact cells and activity for Enzyme II for glucose (Ellglc) of the PTS measured in membrane preparations in the presence of an excess of the soluble PTS proteins in crude cell-free supernatant fractions.(ABSTRACT TRUNCATED AT 250 WORDS)
It was observed in a previous study that the growth of Streptococcus mutans strain OMZ 176 on sorbitol was inhibited by xylitol. The aim of the present study was to investigate the mechanisms involved in this inhibition. It was shown that the uptake of 14C-sorbitol was delayed when the cells had been pre-exposed to xylitol, and that the only labelled substance found intracellularly was sorbitol; no further metabolization occurred. This is in contrast with untreated normal cells, where sorbitol is taken up by a specific phosphotransferase system (pts). The 14C-xylitol metabolism of the cells was qualitatively unchanged in the presence of sorbitol; an intracellular accumulation of 14C-xylitol-phosphate (xylitol-P) and 14C-xylulose-phosphate (xylulose-P) was observed. However, a reduced uptake of xylitol was observed in the presence of sorbitol. Xylitol thus appears to change the pathway by which sorbitol is taken up by the cells. An inducible permease may replace the normal sorbitol pts when xylitol is present. No further metabolization of this intracellular sorbitol seemed to occur in the resting cell suspensions. It was furthermore observed that the presence of sorbitol enhanced the inhibitory potential of xylitol. The accumulation of intracellular sorbitol coincided with markedly increased xylulose-P/xylitol-P ratio. It may be speculated that, if xylulose-P were the major inhibitor of the glycolysis instead of xylitol-P, as previously assumed, an increased concentration of xylulose-P induced by sorbitol could explain that sorbitol enhances the inhibition potential of xylitol. It is not evident, however, how intracellular sorbitol could affect the xylulose-P/xylitol-P ratio.
Sorbitol participates in the osmoregulation of several renal cells and has also been found in isolated inner medullary collecting duct (IMCD) cells in primary culture. Therefore, osmotic regulation and distribution of sorbitol and the key enzymes of sorbitol metabolism, aldose reductase and sorbitol dehydrogenase in the renal inner medulla, were investigated in vivo under various osmotic conditions (control, diuresis, antidiuresis). In homogenates of the renal inner medulla of Wistar rats, the sorbitol content correlated with the urine osmolarity [68 +/- 12 mumol/g protein (control), 28 +/- 9 mumol/g (diuresis), 110 +/- 15 mumol/g (antidiuresis)]. Similar results were obtained for the activity of aldose reductase (sorbitol synthesis) [25 +/- 4 U/g (control), 19 +/- 3 U/g (diuresis), and 48 +/- 7 U/g (antidiuresis)]. On the contrary, the activity of sorbitol dehydrogenase (sorbitol degradation) was significantly increased to 1.26 +/- 0.42 U/g under diuretic conditions vs. control (0.84 +/- 0.14 U/g, P < 0.05). These results demonstrate the correlation between the enzymes of sorbitol synthesis and sorbitol degradation in the intact inner medulla and the urine osmolarity in vivo. Whereas the aldose reductase activity was 2.3-fold enriched in IMCD cells, the specific activity of sorbitol dehydrogenase was relatively increased in a preparation of enriched interstitial cells. This distribution was not dependent on the various diuretic conditions. These results indicate that enzymes of synthesis and of degradation of sorbitol are osmotically regulated in vivo. Therefore, the enzymatic activities of sorbitol synthesis appear to be primarily located in epithelial cells, whereas enzymatic activities of sorbitol degradation seem to be localized in interstitial cells of the renal inner medulla.
-A method for the determination of acid production from 20-25 mg (wet weight) of Streptococcus mutans and 12-33 mg (wet weight) of human dental plaque is described. After endogenous acid production had been followed, either sorbitol or xylitol or a mixture of sorbitol and xylitol (2:1) was added. After about ten minutes glucose, sucrose or Palatinose were added for a vitality test. Addition of xylitol to the bacterial suspension caused inhibition of acid production from sorbitol by Streptococcus mutans grown on sorbitol or a mixture of sorbitol and glucose. It was also observed that it had a similar effect on acid production from sorbitol in suspensions of dental plaque with few exceptions. On the other hand, Streptococcus mutans cells grown on glucose, sucrose and xylitol media, produced no or insignificant amounts of acid from sorbitol. Streptococcus mutans cells grown on media containing glucose, sucrose, sorbitol and a mixture of sorbitol and glucose generally formed a large amount of acid from glucose and sucrose after the addition of sorbitol and xylitol. However, Streptococcus mutans cells grown on a medium containing xylitol and the mixture of sorbitol and xylitol formed less acid from glucose. The acid production activity from sorbitol in suspensions of dental plaque after the xylitol addition was somewhat lower than the acid production from sorbitol alone (p less than 0.02).
Two methods are commonly used to measure sorbitol in mammalian tissues. The first uses sorbitol dehydrogenase for a coupled enzymatic reaction; unfortunately, other polyols are also substrates for this enzyme. The second uses gas-liquid chromatography (GLC) for separation of polyols and mass quantitation of sorbitol. A comparison of these two methods for the measurement of sorbitol in duplicate samples of lens, nerve, and erythrocytes indicates that GLC of polyol acetates consistently finds less sorbitol than measured by sorbitol dehydrogenase. Erythritol, threitol, ribitol, arabitol, and galactitol are polyols found in variable quantities in these tissues, which have a variable influence on the activity of sorbitol dehydrogenase and therefore alter sorbitol quantitation with this enzyme. Moreover, there is an unidentified substance(s) that reacts with sorbitol dehydrogenase which seems to increase in association with hyperglycemia in the lens and nerve, but not in erythrocytes. The quantity of this unknown substance(s) seems to be reduced by the aldose reductase inhibitor sorbinil in erythrocytes and to a lesser extent sciatic nerve and lens. Since enzymatic sorbitol quantitation in the lens, nerve, and erythrocytes is influenced by many known and unknown factors other than sorbitol, we recommend that GLC of polyol acetates be used to measure sorbitol in biologic tissues.