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At least 19 recordsLinked to original sources
PubMed1986

In vivo measurements of sulcal plaque pH after topical applications of sorbitol and sucrose in rats fed sorbitol or sucrose.

To test whether adaptation to sorbitol could be observed in rat plaque, we made pH measurements of rat sulcal plaque in vivo, following topical application of 10% sorbitol solution. Rat pups were inoculated orally with S. mutans 6715 and fed diet MIT 305 (5% sucrose) for 16 days. Baseline sulcal plaque pH response of these rats to topical application of 10% sorbitol solution was measured. One group of 16 rats was then fed 20% sucrose in the diet, and a second group 20% sorbitol. After 13 days' feeding of the experimental diets (four days were used for accommodation to dose, and nine days at the 20% level for sorbitol), there was a significantly greater (p less than 0.01) drop in pH following topical application of 10% sorbitol in this group than in the sucrose-fed group. There was no difference in the pH response of the two groups to topical application of a 10% sucrose solution when tested six days later. The sulcal enamel caries score was significantly higher (p less than 0.001) in the sucrose group, but buccal enamel scores were similar in both groups. Adaptation in rat plaque took place, and could be measured in vivo as an increased drop in sulcal plaque pH following topical application of sorbitol. It is not clear whether this adaptation was primarily due to selection of sorbitol-fermenting micro-organisms, or, more likely, by induction of sorbitol-specific enzymes. Relative to the sucrose-containing diet, the sorbitol diet was hypocariogenic, even under experimental conditions.

Administration, Topical↗
PubMed1988

Human erythrocyte sorbitol metabolism and the role of sorbitol dehydrogenase.

Rapid fluctuation of erythrocyte sorbitol in response to the changes in plasma glucose concentration has been reported from clinical evidence. We performed more extensive in vitro and in vivo studies focussing on how fast sorbitol was accumulated and how fast the accumulated sorbitol was oxidised in response to the changes in ambient glucose concentration. Incubation studies of intact erythrocytes from healthy subjects and diabetic patients showed that erythrocyte sorbitol increased rapidly in response to increased ambient glucose concentration and the accumulated sorbitol easily decreased according to the rapid reduction of ambient glucose concentration. In addition, the higher the glucose concentration in the medium, the more erythrocytes could accumulate sorbitol. The rapid response of sorbitol levels to ambient glucose concentration was further confirmed by the results of a 75 g oral glucose tolerance test in non-diabetic subjects and diabetic patients with gastrectomy, who showed marked early hyperglycaemia caused by rapid absorption of ingested glucose and subsequent rapid reduction of plasma glucose concentration (erythrocyte sorbitol levels changed concomitantly). These findings strongly indicate that the measurement of erythrocyte sorbitol is not useful as an index of medium or long term glycaemic control.

Adult↗
PubMed1986

Sorbitol concentrations in plasma in connection with transurethral resection of the prostate using sorbitol solution as an irrigating fluid.

20 patients undergoing transurethral resection of the prostate (TURP) using 5% sorbitol (N = 13) or Cytosol (N = 7) (5% sorbitol and 0.25% acetic acid) as an irrigating fluid were studied. The sorbitol concentration was determined in serum (plasma), as were sodium, prostatic acid phosphatase protein (PAP) and osmolality, as possible indicators of absorption of irrigating fluid. The plasma level of sorbitol immediately postoperatively, the increase in serum PAP and the decrease in serum sodium all reflect the amount of irrigating fluid absorbed during TURP. The three variables are intercorrelated. The plasma osmolality was not significantly changed. The maximum sorbitol concentration immediately postoperatively in any patient was 6.0 g/l (33.5 mmol/l). The mean for the series was 1.2 g/l (6.8 mmol/l). The mean serum PAP increase was 31 micrograms/l. The serum sodium decrease ranged between 0 and 14 mmol/l, mean 5.0 mmol/l. The mean half-life of sorbitol in plasma was short: 35 min, reflecting rapid metabolism. An estimate of the volume of fluid absorbed was made from the plasma sorbitol levels observed. A fluid absorption up to 2.3 l (mean 0.6 l) was found. A marked diuretic effect up to 14.1 ml/min (mean 7.8 ml/min) was observed in some cases when irrigation with sorbitol was combined with intravenous furosemide given postoperatively.

Aged↗
PubMed1986

Three-generation reproduction study of rats ingesting up to 10% sorbitol in the diet--and a brief review of the toxicological status of sorbitol.

Groups of 12 male and 24 female 5-wk-old Charles River CD (SD) BR rats (F0) were fed a sucrose-containing ground cereal-based diet in which 0, 2.5, 5.0 and 10.0% (w/w) sorbitol was included at the expense of sucrose. The rats were first mated after 14 wk on the diet. F1a litters were born 19 wk after the start of the study and F1b litters at wk 30. Groups of 12 male and 24 female F1b rats were first mated when 18 wk old. They gave rise to F2a litters after 3 wk and to F2b litters 10 wk later. Likewise, groups of 12 male and 24 female F2b rats were first mated when 18 wk old, producing F3a and F3b litters 3 wk and 10 wk later, respectively. F0 rats were killed 33 wk after the start of the study, F1a in wk 22, F1b in wk 68, F2a in wk 57, F2b in wk 92 and F3a in wk 96. Apart from slight reductions in food consumption in sorbitol-fed F1b males and in body-weight gain in sorbitol-fed F0, F1b and F2b rats of both sexes, treatment was associated with no clinically observed effects. There were no deaths attributable to treatment and no adverse effects on mating performance or pregnancy rates in the parent animals of any generation. Treatment was associated with no consistent adverse effect on any measure of reproductive performance or behaviour during gestation or lactation. No abnormal pups were observed in any generation. Not unexpectedly, caecal enlargement was consistently observed at necropsy of sorbitol-treated rats of all generations and significant rises in serum calcium were observed in F0 males and females exposed to 10% sorbitol and in F1b males exposed to either 5 or 10% sorbitol. Differences between treated and control F3a rats in respect of T3 and TSH levels were probably spurious as they followed no consistent pattern. Similarly, between-group variations in gonadal weight were considered to have no toxicological significance because they lacked consistency and were not accompanied by any histologically-evident changes. Microscopic examination of lesions from F1a and F2a animals, of gonads from F1b and F2b and of selected tissues from the F3a generation revealed no changes of toxicological significance.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Medulla↗
PubMed1988

Functional bowel disease: malabsorption and abdominal distress after ingestion of fructose, sorbitol, and fructose-sorbitol mixtures.

Twenty-five patients with functional bowel disease were given fructose, sorbitol, fructose-sorbitol mixtures, and sucrose. The occurrence of malabsorption was evaluated by means of hydrogen breath tests and the gastrointestinal symptoms, if any, were recorded. One patient could not be evaluated because of lack of H2 production. Based on a cut-off level of 10 ppm rise of H2 concentration, malabsorption was apparent in 13 patients, in 7 of which the calculated absorption capacities were below 15 g. In contrast, in patients given 50 g of sucrose, malabsorption could not be detected. Ingestion of fructose caused marked abdominal distress in patients with demonstrable malabsorption. Ingestion of sucrose in these patients gave less pronounced symptoms of abdominal distress. Malabsorption of a 5-g dose of sorbitol could be detected in 8 of 13 patients. Mixtures of 25 g of fructose and 5 g of sorbitol caused significantly increased abdominal distress, and more than additive malabsorption was found in several cases. The present study shows that pronounced gastrointestinal distress may be provoked by malabsorption of small amounts of fructose, sorbitol, and fructose-sorbitol mixtures in patients with functional bowel disease. The findings may have direct influence on the dietary guidance given to a major group of patients with functional bowel disease and may make it possible to define separate entities in this disease complex.

Adult↗
PubMed1990

Sorbitol-fermenting predominant cultivable flora of human dental plaque in relation to sorbitol adaptation and salivary secretion rate.

The sorbitol-fermenting predominant flora of human dental plaque was studied in 12 people with low and 11 with normal salivary secretion rates before and after a period of frequent mouth rinses with sorbitol solution. A total of 277 sorbitol-fermenting isolates are described by their morphological and physiological characteristics. The flora was almost exclusively composed of gram-positive bacteria belonging to the genera Streptococcus, Lactobacillus and Actinomyces in people with low secretion rates and Streptococcus and Actinomyces in those with normal salivation. At the species level, Streptococcus mutans predominated in all. The frequent use of sorbitol resulted in an increase of the streptococcal species mainly and particularly of Streptococcus sanguis I in people with normal salivation. The counts of lactobacilli and Actinomyces remained unaffected. Almost all isolates appeared to belong to the resident plaque flora. Succession of new sorbitol-fermenting genera to the plaque community could not be observed as a result of the frequent exposure of the mouth to sorbitol.

Adaptation, Biological↗
PubMed1976

The sorbitol pathway: effect of streptozotocin induced diabetes and the feeding of a sucrose-rich diet on glucose, sorbitol and fructose in the retina, blood and liver of rats.

The sorbitol, fructose and glucose content of the retina, blood and liver from normal and streptozotocin diabetic rats fed either a starch- or sucrose-rich diet for 15 days has been determined. The sorbitol and fructose level in the retina was much higher than that in either the liver or blood and was significantly increased in diabetes on either diet. Such increases in the sorbitol concentration did not occur in either the liver or the blood during diabetes, and the possibility that the sorbitol pathway can play an important metabolic role in the diabetic retina has been discussed. The feeding of a sucrose- as opposed to a starch-rich diet did not significantly alter the concentrations of glucose, sorbitol or fructose in the normal rat retina but caused a marked elevation in the diabetic state.

Animals↗
PubMed1979

[Influence in vivo of sorbitol on sorbitol dehydrogenase activity].

Previous researches carried out on the metabolism of sorbitol in the rat showed the influence of this polyalcohol on the activity of some dehydrogenases NAD and NADP-dependent and on lacate/pyruvate, NADH/NAD and NADPH/NADP ratios. Since sorbitol dehydrogenase (SDH, EC 1.1.1.14) is an enzyme with a great affinity for sorbitol, it seemed interesting to investigate the effect of a sorbitol-enriched diet on SDH activity in the rat liver after different periods of dietary treatment (20, 40, 60 days). SDH was assayed by a continuous optical test according to Bücher et al. The data obtained show a repressive action on SDH activity by a sorbitol-enriched diet. In fact, whilst after 20 days of treatment SDH activity decreased of about 18% in respect of the controls, after 60 days a decrease of 80% was observed. This result is so interesting to stimulate other investigations in vitro on the kinetics of such metabolic reaction in the attempt to explain the relation between the enzyme and its substrate.

Animals↗
PubMed1976

[Parenteral administration of sorbitol solution and its impact on sorbitol, glucose, fructose and lactate concentration in the blood of cattle, sheep and piglets].

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.

Animals↗
PubMed1991

Sorbitol transport by Streptococcus sanguis 160.

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)

Dental Plaque↗
PubMed1991

Sorbitol transport and metabolism by oral streptococci.

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.

Acetyltransferases↗
PubMed1989

A novel sorbitol transport mechanism in cultured renal papillary epithelial cells.

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.

Animals↗
PubMed1991

Sorbitol inhibition of glucose metabolism by Streptococcus sanguis 160.

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)

Dental Plaque↗
PubMed1986

Sorbitol increases the growth inhibition of xylitol on Strep. mutans OMZ 176.

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.

Biological Transport↗
PubMed1992

Measurements of tissue sorbitol in diabetes mellitus: enzyme method versus gas-liquid chromatography.

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.

Aldehyde Reductase↗