Absorption, Distribution and Excretion
Chemical changes in the blood induced by maltitol were compared with those induced by glucose in both healthy people and patients with several disorders, including diabetes mellitus. Blood glucose levels of healthy subjects were determined after the administration of glucose (12.5, 25, or 50 g) or maltitol (50 g). Based on the glucose absorption curve, 38% of the maltitol that was orally administered was absorbed through the intestinal tract, but the absorption of maltitol was more delayed than that of glucose.
Pieces of New Zealand rabbit small intestine were everted and incubated with 100 mM substrate (maltitol, sucrose, or glucose). After removal at different times (20, 40, or 60 min.) of incubation, the volume of serosal fluid and the dry mass of the gut pieces were determined. Maltitol was hydrolyzed, and the hydrolysis products were absorbed by the everted sacs. No maltitol was detected in the serosal fluid. The serosal glucose concentration increased at a slower rate after incubation with maltitol than after incubation with glucose or sucrose. The rate of hydrolysis and absorption decreased with the longer time of incubation.
In an in vitro study of (14)C-U-maltitol in everted intestinal sacs, the highest transport of (14)C-maltitol was displayed in the jejunum, followed by the ileum and duodenum. Twenty-four hr after oral administration of (14)C-U-maltitol, 60% of the radioactivity was detected in the cecum, large intestine, and feces. Five percent was excreted in the urine and 1.2% was expired as CO2 within 24 hr. When (14)C-U-maltitol was injected i.v., over 35, 60, and 85% of the administered dose was excreted in the urine within 1, 3, and 24 hr, respectively.
Two male beagle dogs were given maltitol-U-(14)C (51.2 uCi) by stomach tube. Blood samples were collected until 32 hr after dosing. The peak radiolabel concentration in plasma was 2 hr after maltitol administration (304 and 263 ug/mL, expressed as maltitol equivalent in the 2 dogs). The radioactivity present in the urine after 48 hr was 7.8 and 3.8% of the administered dose in the 2 animals.
For more Absorption, Distribution and Excretion (Complete) data for Maltitol (11 total), please visit the HSDB record page.

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Metabolism / Metabolites
The metabolism of maltitol (4-alpha-D-glucosylsorbitol) was assessed in fasting conventional (C) rats, C mice and germ-free (GF) mice, using [U-14C]maltitol. The radiorespirometric patterns of (14)CO2 collected for 48 hr after the administration of labelled maltitol were characterized by a constant rate of (14)CO2 production lasting 4 hr for both C rats and mice. The pattern for the GF mice showed a peak at the second hour followed immediately by a slow decrease. The percentage recovery of (14)CO2 was significantly lower for the GF mice (59%) compared with C animals (72-74%). Urine, feces and intestinal contents after 48 hr totalled 19% of the administered radioactivity in the C rats and mice and 39% in the GF mice. The digestibility of maltitol and the absorption of sorbitol in GF mice was also assessed. The cecum and small intestine of GF mice, 3 hr after administration of equimolar quantities of maltitol (140 mg/kg body-weight) or sorbitol (70 mg/kg body-weight), contained 39 and 51% of the ingested dose respectively, present mostly in the cecum as sorbitol. The alpha-glucosidase (maltase) activity of the small intestine was appreciably higher (1.5-1.7 times) in the GF mice than in the C mice. These results suggest that the enzymic activities in the small intestine of mice and rats are sufficient to hydrolyse maltitol extensively. Consequently, the slow absorption of sorbitol seems to be an important factor limiting the overall assimilation of maltitol in the small intestine.
Conventional (CV) rats were given a single oral dose of 1 or 2 g maltitol. Urine and faeces were collected during the following 24 hr and their contents of maltitol and sorbitol were measured. Very little of either substance appeared in the faeces but appreciable amounts of sorbitol found in the urine indicated that the maltitol had been hydrolysed. Excretion of maltitol and sorbitol was compared in germ-free and CV rats given an oral dose of 2 g maltitol. Significantly less of both substances was recovered in the faeces of CV rats, but urinary excretion was similar in both environments. Maltitol injected intravenously gave rise to only traces of sorbitol in the excreta. A dose of 250 mg was cleared almost completely from the circulation within 1 hr. It is concluded that maltitol is hydrolysed by animal tissues, either in the gut lumen before absorption or in the gut wall during absorption. Maltitol and sorbitol are also degraded by gut bacteria, mostly in sites distal to the main absorptive area. The contribution to the host's nutrition would depend on the extent to which the end-products of fermentation are absorbed from the colon.
Weanling Wistar rats placed on diets containing 13 or 26% maltitol for 9 weeks had reduced body-weight gains and increased intestinal weights as compared with controls. Enzymatic tests in dosed rats indicated that the alpha-glycosidic linkage of maltitol was not hydrolysed with pancreatic enzymes or enzymes of the intestinal mucosa. Maltitol dehydrogenase was not observed in liver-cell cytoplasm and prolonged maltitol administration did not induce hepatic sorbitol dehydrogenase.

Interactions
The effects of maltitol and mannitol on the /gastrointestinal/ absorption of acetaminophen, sulfisoxazole and riboflavin in mice were investigated in a controlled double-blind fashion. Oral maltitol or mannitol was administered to 6 mice and 2 hr after ingestion the blood levels of the 3 drugs were found to be lower than in the controls, and drug absorption was inhibited. It was suggested that these results were caused by the action of maltitol and mannitol which accelerated small intestine motility, secretion and vascular permeability in the intestinal membrane. These changes may be mediated by biogenic amine, serotonin, histamine and polyamines in the small intestine.
To estimate the suppressive effect of partially hydrolyzed guar gum (PHGG) on transitory diarrhea induced by ingestion of a sufficient amount of maltitol or lactitol in female subjects. The first, the minimal dose level of maltitol and lactitol that would induce transitory diarrhea was estimated separately for each subject. Individual subject was administered a dose that increased by 5 g stepwise from 10 to 45 g until diarrhea was experienced. Thereafter, the suppressive effect on diarrhea was observed after each subject ingested a mixture of 5 g of PHGG and the minimal dose level of maltitol or lactitol. Thirty-four normal female subjects (21.3+/-0.9 years; 49.5+/-5.3 kg). Incidence of diarrhea caused by the ingestion of maltitol or lactitol and the ratio of suppression achieved by adding PHGG for diarrhea. The ingestion of amounts up to 45 g of maltitol, diarrhea caused in 29 of 34 subjects (85.3%), whereas the ingestion of lactitol caused diarrhea in 100%. The diarrhea owing to maltitol was improved in 10 of 28 subjects by the addition of 5 g of PHGG to minimal dose-induced diarrhea, and that owing to lactitol was in seven of 19 subjects. Adding 10 g of PHGG strongly suppressed the diarrhea caused by maltitol, and the cumulative ratio was 82.1% (23/28). The transitory diarrhea caused by the ingestion of maltitol or lactitol was clearly suppressed by the addition of PHGG. These results strongly suggest that diarrhea caused by the ingestion of a sufficient amount of non-digestible sugar substitute can be suppressed by the addition of dietary fiber.
The enhancing effects of maltitol (alpha-D-glucopyranosyl-1,4-sorbitol) on absorption of calcium by the rat intestine have been studied by use of [(45)Ca]CaCl2 in-vivo. After intragastric administration of [(45)Ca]CaCl2 solution with maltitol, plasma (45)Ca concentration remained at the maximum level for more than 80 min, whereas for animals given [(45)Ca]CaCl2 solution without maltitol, plasma (45)Ca concentration declined sharply after the peak. Determination of (45)Ca radioactivity remaining in the various segments of the gastrointestinal tract revealed that administration of maltitol elicited slower gastric emptying and slower intestinal transit, resulting in extensive (45)Ca distribution along the small intestine throughout the experimental period. The luminal contents of the small intestine were significantly higher in rats given maltitol than in the control group. These results suggest that the enhancing action of maltitol on intestinal calcium absorption could be attributed to reduced gastrointestinal calcium transit and increased luminal fluid content, presumably because of the osmotic activity of maltitol; this would not only accelerate the dissolution of calcium into the increased luminal contents, but also enable a larger area of the small intestine to absorb calcium for a longer period of time.
Dental caries and periodontal disease are wide-spread oral illnesses whose etiology is intimately associated with the consumption of carbohydrate sweeteners. ...Human clinical trials and several animal experiments have shown promising clinical results obtained by replacing sucrose with certain sugar alcohols (polyols). Among the sugar alcohols, the best results so far have been obtained with xylitol, which is chemically a pentitol containing five carbon atoms. Chewing gums containing xylitol have been shown to be strong instruments against caries in caries-active age-groups and in high-risk subjects. More research is needed to assess the ability of mixtures of xylitol with sorbitol, palatinit, maltitol, other sugar alcohols, and intense sweeteners to prevent oral plaque diseases. Although thorough clinical trials on the relationship between carbohydrate sweeteners and periodontal diseases have not been performed, the available data indicate that dietary polyols may have a restricted dampening effect on periodontal and gingival inflammations.

[1]. Application A537 – Reduction in the energy factor assigned to Maltitol: Final Assessment Report (PDF), Food Standards Australia New Zealand, 5 October 2005, retrieved 27 January 2014.

Maltitol is an alpha-D-glucoside consisting of D-glucitol having an alpha-D-glucosyl residue attached at the 4-position. Used as a sugar substitute. It has a role as a metabolite, a laxative and a sweetening agent. It is an alpha-D-glucoside and a glycosyl alditol. It is functionally related to an alpha-D-glucose and a D-glucitol.
Maltitol has been reported in Lotus burttii, Lotus tenuis, and other organisms with data available.

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Mechanism of Action
... Reports from authoritative bodies and reviews indicates that the decrease in pH in plaque as a consequence of metabolic acid production by saccharolytic bacteria when exposed to fermentable carbohydrates (i.e. sugars and starches) may promote demineralization and prevent remineralization of the hydroxyapatite crystals. Tooth hydroxyapatite crystals are very resistant to dissolution at neutral pH, but their solubility drastically increases as pH drops. Typically, the critical pH for dental enamel is around 5.5. ... Demineralization of tooth tissues can also occur as a result of consumption of dietary acids in foods or beverages, and that frequent consumption can lead to dental erosion. Xylitol, sorbitol, mannitol, maltitol, lactitol, isomalt, erythritol, D-tagatose, isomaltulose, sucralose and polydextrose are slowly metabolized by bacteria in the mouth. The rate and amount of acid production from these food constituents is significantly less than that from sucrose. ... Xylitol, sorbitol, mannitol, maltitol, lactitol, isomalt, erythritol, D-tagatose, isomaltulose, sucralose and polydextrose do not promote dental caries because they do not lower plaque pH to the level associated with enamel demineralization. ... A cause and effect relationship has been established between the consumption of sugar-containing foods/drinks at an exposure frequency of four times daily or more and an increased tooth demineralization, and that the consumption of foods/drinks containing xylitol, sorbitol, mannitol, maltitol, lactitol, isomalt, erythritol, D-tagatose, isomaltulose, sucralose or polydextrose, instead of sugar in sugar-containing foods/drinks, may maintain tooth mineralization by decreasing tooth demineralization compared with sugar-containing foods, provided that such foods/drinks do not lead to dental erosion.
The food constituents xylitol, sorbitol, mannitol, maltitol, lactitol, isomalt, erythritol, D-tagatose, isomaltulose, sucralose or polydextrose resulted in reduced post-prandial blood glucose (or insulinemic) responses compared with sugars on a weight by weight basis owing to their reduced/delayed digestion/absorption and/or to a decrease in the amount of available carbohydrates, and that the consumption of foods/drinks in which xylitol, sorbitol, mannitol, maltitol, lactitol, isomalt, erythritol, D-tagatose, isomaltulose, sucralose or polydextrose replaced sugars induced lower post-prandial glycemic and insulinemic responses than sugar-containing foods/drinks. ... A cause and effect relationship has been established between the consumption of foods/drinks containing xylitol, sorbitol, mannitol, maltitol, lactitol, isomalt, erythritol, D-tagatose, isomaltulose, sucralose or polydextrose instead of sugar and reduction in post-prandial blood glucose responses (without disproportionally increasing post-prandial insulinemic responses) as compared to sugar-containing foods/drinks.

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Therapeutic Uses
Sugar Alcohols; Maltose/analogs & derivatives; Sweetening Agents

C12H24O11

344.3124

344.131

585-88-6

493591

White to off-white solid powder

1.7±0.1 g/cm3

788.5±60.0 °C at 760 mmHg

149-152 °C(lit.)

430.7±32.9 °C

0.0±6.2 mmHg at 25°C

1.634

-5.14

9

11

8

23

343

9

C([C@@H]1[C@H]([C@@H]([C@H]([C@H](O1)O[C@H]([C@@H](CO)O)[C@@H]([C@H](CO)O)O)O)O)O)O

VQHSOMBJVWLPSR-WUJBLJFYSA-N

InChI=1S/C12H24O11/c13-1-4(16)7(18)11(5(17)2-14)23-12-10(21)9(20)8(19)6(3-15)22-12/h4-21H,1-3H2/t4-,5+,6+,7+,8+,9-,10+,11+,12+/m0/s1

(2S,3R,4R,5R)-4-[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyhexane-1,2,3,5,6-pentol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~33.33 mg/mL (~96.80 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.26 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (7.26 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (7.26 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)