Absorption, Distribution and Excretion
This study compared the blood chemistry changes induced by maltitol and glucose in healthy individuals and patients with various diseases, including diabetes. Blood glucose levels were measured after healthy subjects received either glucose (12.5, 25, or 50 g) or maltitol (50 g). According to glucose absorption curves, 38% of orally administered maltitol was absorbed via the intestine, but at a slower rate than glucose. The small intestine of New Zealand rabbits was inverted and incubated with a 100 mM substrate (maltitol, sucrose, or glucose). Intestinal segments were removed at different incubation times (20, 40, or 60 minutes) to measure serous fluid volume and dry weight. Maltitol underwent hydrolysis, and the hydrolysis products were absorbed by the inverted intestinal pouch. Maltitol was not detected in the serous fluid. Compared to glucose or sucrose incubation, the increase in serous glucose concentration after maltitol incubation was slower. The rates of hydrolysis and absorption decreased with increasing incubation time.
In in vitro studies of (14)CU-maltitol in the inverted intestinal sac, (14)C-maltitol showed the highest translocation in the jejunum, followed by the ileum and duodenum. Twenty-four hours after oral administration of (14)CU-maltitol, 60% of the radioactivity was detected in the cecum, large intestine, and feces. 5% was excreted in the urine, and 1.2% was excreted as carbon dioxide within 24 hours. Following intravenous administration of (14)Cu-maltitol, more than 35%, 60%, and 85% of the administered dose were excreted in the urine within 1, 3, and 24 hours, respectively.
Two male beagle dogs were administered maltitol-U-(14)C (51.2 μCi) via gastric tube. Blood samples were collected within 32 hours post-administration. Peak concentrations of the radiolabeled radionuclide in plasma occurred at 2 hours post-administration (304 and 263 μg/mL in the two dogs, respectively, expressed as maltitol equivalents). The radioactivity in the urine of the two animals 48 hours after administration was 7.8% and 3.8% of the administered dose, respectively. For more complete data on the absorption, distribution, and excretion of maltitols (11 in total), please visit the HSDB record page. Metabolism/Metabolites This study used [U-14C]maltitol to assess the metabolism of maltitol (4-α-D-glucosylsorbitol) in fasted conventional (C) rats, C mice, and germ-free (GF) mice. Radioactive respiration patterns of (14)CO2 collected within 48 hours after administration of labeled maltitol showed that the (14)CO2 production rate in C rats and mice remained constant over 4 hours. Patterns in GF mice showed a peak at the second hour, followed by an immediate and slow decline. The recovery rate of ¹⁴CO_sub>2 in germ-free (GF) mice was significantly reduced (59%) compared to the control group (C group) animals (72-74%). Forty-eight hours later, the total radioactivity in the urine, feces, and intestinal contents of control rats and mice accounted for 19% of the total administered dose, while it was 39% in germ-free mice. Furthermore, the digestibility of maltitol and the absorption of sorbitol in germ-free mice were assessed. Three hours after administration of equimolar amounts of maltitol (140 mg/kg body weight) or sorbitol (70 mg/kg body weight) to germ-free mice, 39% and 51% of the ingested dose were present in the cecum and small intestine, respectively, with the majority in the cecum as sorbitol. The α-glucosidase (maltase) activity in the small intestine of germ-free mice was significantly higher than that in control mice (1.5–1.7 times). These results indicate that the enzyme activity in the small intestine of mice and rats is sufficient to adequately hydrolyze maltitol. Therefore, slow sorbitol absorption appears to be an important factor limiting the overall absorption of maltitol by the small intestine.
Conventional (CV) rats were administered a single oral dose of 1 or 2 grams of maltitol. Urine and feces were collected over the following 24 hours, and the levels of maltitol and sorbitol were determined. The levels of both substances in feces were extremely low, but a significant amount of sorbitol was detected in urine, indicating that maltitol had been hydrolyzed. Maltitol and sorbitol excretion was compared between germ-free rats and conventional rats orally administered 2 g maltitol. The recovery of both substances in feces was significantly reduced in conventional rats, but urinary excretion was similar in both environments. Following intravenous injection of maltitol, only trace amounts of sorbitol were detected in the excrement. A dose of 250 mg was almost completely cleared from the circulatory system within 1 hour. It is concluded that maltitol is hydrolyzed in animal tissues, and this hydrolysis may occur in the intestinal lumen before absorption or in the intestinal wall during absorption. Maltitol and sorbitol are also degraded by intestinal bacteria, primarily in areas far from the main absorption area. Their contribution to host nutrition depends on the extent to which fermentation end products are absorbed from the colon. After weaning, Wistar rats fed diets containing 13% or 26% maltitol for 9 weeks showed reduced weight gain and increased intestinal weight compared to the control group. Enzymatic tests on the treated rats showed that the α-glycosidic bond of maltitol could not be hydrolyzed by pancreatic enzymes or intestinal mucosal enzymes. Maltitol dehydrogenase was not observed in the hepatocyte cytoplasm, and long-term administration of maltitol did not induce the expression of hepatic sorbitol dehydrogenase.

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- Absorption: Maltitol is partially absorbed in the small intestine via sodium-glucose cotransporter (SGLT). In humans, the absorption rate is approximately 50% to 60% of the ingested dose. Unabsorbed maltitol enters the large intestine [1].
- Metabolism: Absorbed maltitol is transported to the liver, where it is metabolized to sorbitol by maltitol dehydrogenase and further converted to glucose by sorbitol dehydrogenase. A small amount is metabolized to fructose. Maltitol is metabolized more slowly than glucose, and therefore has a lower glycemic response [1]
- Excretion: The metabolites of maltitol (glucose, sorbitol, fructose) are mainly excreted through urine. Unabsorbed maltitol is fermented by intestinal flora in the large intestine to produce short-chain fatty acids (SCFAs), gases (hydrogen, carbon dioxide, methane) and water; the short-chain fatty acids are absorbed and used for energy, while the gases are expelled through flatulence [1]

Interactions
This study employed a double-blind, controlled trial to investigate the effects of maltitol and mannitol on the absorption of acetaminophen, sulfamethoxazole, and riboflavin in the gastrointestinal tract of mice. Six mice were orally administered maltitol or mannitol. Two hours later, the concentrations of these three drugs in the blood of the mice were lower than in the control group, and drug absorption was inhibited. The study suggests that these results may be due to maltitol and mannitol accelerating small intestinal motility, secretion, and intestinal vascular permeability. These changes may be mediated by biogenic amines, serotonin, histamine, and polyamines in the small intestine. This study also evaluated the inhibitory effect of partially hydrolyzed guar gum (PHGG) on transient diarrhea induced in women by adequate intake of maltitol or lactitol. First, the minimum dose of maltitol and lactitol to induce transient diarrhea was estimated for each subject. The dose for each subject was gradually increased from 10 g to 45 g in increments of 5 g until diarrhea occurred. The study then observed the inhibitory effect of PHGG on diarrhea after each subject ingested a mixture of 5g PHGG and the minimum dose of maltitol or lactitol. The study included 34 healthy female subjects (age 21.3 ± 0.9 years; weight 49.5 ± 5.3 kg). Results included the incidence of diarrhea induced by maltitol or lactitol intake and the inhibitory rate of diarrhea induced by PHGG. After ingesting up to 45g maltitol, 29 of the 34 subjects (85.3%) experienced diarrhea, while lactitol intake resulted in diarrhea in 100% of the subjects. Of the 28 subjects, 10 experienced diarrhea due to maltitol intake, and their symptoms improved after adding 5g PHGG to the minimum dose-induced diarrhea; of the 19 subjects, 7 experienced diarrhea due to lactitol intake, and their symptoms improved. Adding 10g PHGG significantly inhibited maltitol-induced diarrhea, with a cumulative inhibition rate of 82.1% (23/28). The addition of PHGG significantly inhibited transient diarrhea induced by maltitol or lactitol intake. These results strongly suggest that diarrhea caused by adequate intake of indigestible sugar substitutes can be inhibited by adding dietary fiber. The promoting effect of maltitol (α-D-glucopyranosyl-1,4-sorbitol) on intestinal calcium absorption in rats was studied in vivo using [(45)Ca]CaCl2. After intragastric administration of a solution containing maltitol [(45)Ca]CaCl2, plasma (45)Ca concentration remained at its highest level for more than 80 minutes; while in animals not administered the solution, plasma (45)Ca concentration rapidly decreased after reaching its peak. Measurement of residual (45)Ca radioactivity in different segments of the gastrointestinal tract revealed that maltitol administration slowed gastric emptying and intestinal transit, resulting in widespread distribution of (45)Ca in the small intestine throughout the experiment. Compared with the control group, rats given maltitol showed a significant increase in small intestinal contents. These results suggest that the promoting effect of maltitol on intestinal calcium absorption may be attributed to slowed gastrointestinal calcium transport and increased intestinal fluid volume, possibly due to the osmotic activity of maltitol. This not only accelerates calcium dissolution in the increased intestinal contents but also allows a larger area of the small intestine to absorb calcium over a longer period. Dental caries and periodontal disease are common oral diseases, and their etiology is closely related to the intake of carbohydrate sweeteners. …Human clinical trials and multiple animal studies have shown that replacing sucrose with certain sugar alcohols (polyols) can yield encouraging clinical results. Among these sugar alcohols, xylitol, a five-carbon pentose alcohol, has been the most effective to date. Xylitol-containing chewing gum has been shown to be an effective tool for preventing dental caries in high-risk and high-prevalence age groups. Further research is needed to evaluate the ability of xylitol in combination with sorbitol, palatinib, maltitol, other sugar alcohols, and potent sweeteners to prevent dental plaque disease. Although no comprehensive clinical trials have been conducted on the relationship between carbohydrate sweeteners and periodontal disease, existing data suggest that dietary polyols may have some inhibitory effect on periodontal and gingival inflammation.

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- Acute toxicity: maltitol has low acute toxicity. In rodent studies, the oral median lethal dose (LD₅₀) was greater than 20 g/kg body weight (bw), indicating no risk of acute toxicity at normal dietary intake levels [1]
- Subchronic toxicity: In a 90-day subchronic rat study, oral administration of maltitol at doses up to 1000 mg/kg bw/day did not show any adverse effects on body weight, food intake, hematological parameters, clinical chemistry indicators (including liver and kidney function indicators), or organ weight. No Observed Adverse Effects (NOAEL) was determined to be 1000 mg/kg body weight/day [1]
- Gastrointestinal side effects: High doses may cause osmotic diarrhea, bloating, flatulence and abdominal cramps due to unabsorbed maltitol in the large intestine. In humans, these side effects usually occur when the daily intake exceeds 30-50 g; the severity is dose-related and varies from person to person [1]
- Dental safety: Maltitol is not cariogenic. It is not fermented by oral bacteria (such as Streptococcus mutans) to produce acids that cause demineralization of tooth enamel and therefore does not cause tooth decay [1]

[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 α-D-glucosinolate, consisting of D-glucol with an α-D-glucose residue linked at the 4-position. It is used as a sugar substitute. Maltitol has metabolic, laxative, and sweetener effects. It is an α-D-glucosinolate and a glycosyl aldosterone. Its functions are related to α-D-glucose and D-glucol. Maltitol has been reported to be found in Lotus burttii, Lotus tenuis, and other organisms with relevant data. Mechanism of Action…Reports and reviews from authoritative institutions indicate that when glycolytic bacteria in dental plaque are exposed to fermentable carbohydrates (i.e., sugars and starches), the acids produced by metabolism cause a decrease in the pH of the plaque, which may promote the demineralization of hydroxyapatite crystals and prevent their remineralization. Tooth hydroxyapatite crystals are highly resistant to dissolution at neutral pH, but their solubility increases sharply as the pH decreases. Typically, the critical pH for tooth enamel is approximately 5.5. Dietary acids in food and beverages can also cause tooth demineralization, and frequent intake can lead to tooth erosion. Xylitol, sorbitol, mannitol, maltitol, lactitol, isomaltulose, erythritol, D-tagatose, isomaltulose, sucralose, and polydextrose are slowly metabolized by oral bacteria. These food components produce acids at a much lower rate and in much smaller quantities than sucrose. Xylitol, sorbitol, mannitol, maltitol, lactitol, isomaltulose, erythritol, D-tagatose, isomaltulose, sucralose, and polydextrose do not promote tooth decay because they do not lower the pH of dental plaque to levels associated with enamel demineralization. Studies have shown a causal relationship between consuming sugary foods/beverages four or more times daily and increased tooth demineralization. Furthermore, if sugar in sugary foods/beverages is replaced with xylitol, sorbitol, mannitol, maltitol, lactitol, isomaltulose, erythritol, D-tagatose, isomaltulose, sucralose, or polydextrose, tooth mineralization may be maintained by reducing tooth demineralization, provided these foods/beverages do not cause tooth erosion. Compared to sugars, food ingredients such as xylitol, sorbitol, mannitol, maltitol, lactitol, isomaltulose, erythritol, D-tagatose, isomaltulose, sucralose, or polydextrose, by weight, can reduce postprandial glycemic (or insulin) response. Because of reduced/delayed digestion/absorption and/or reduced availability of carbohydrates, consuming foods/beverages that replace sugars with xylitol, sorbitol, mannitol, maltitol, lactitol, isomaltulose, erythritol, D-tagatose, isomaltulose, sucralose, or polydextrose results in lower postprandial blood glucose and insulin responses compared to consuming sugary foods/beverages. Studies have shown that consuming foods/beverages containing xylitol, sorbitol, mannitol, maltitol, lactitol, isomaltulose, erythritol, D-tagatose, isomaltulose, sucralose, or polydextrose (rather than sugars) reduces postprandial blood glucose responses (without disproportionately increasing postprandial insulin responses) compared to consuming sugary foods/beverages.

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Therapeutic Uses
Sugar alcohols; maltose/analytes and derivatives; sweeteners - Background: Maltitol is a sugar alcohol (polyol) used as a low-calorie sweetener and filler in food. It is produced by hydrogenation of maltose, which is derived from starch hydrolysis [1]. - Energy Factor Adjustment: The final assessment report recommends reducing the energy factor of maltitol from 10 kJ/g (2.4 kcal/g) to 8.4 kJ/g (2.0 kcal/g). This adjustment is based on its partial absorption, slow metabolism, and the fermentation of unabsorbed portions, resulting in a lower net energy availability than sucrose (17 kJ/g) [1]. - Food Applications: Maltitol is widely used in sugar-free or low-sugar foods, including chewing gum, candy, baked goods, ice cream, and dietary supplements. Its sweetness is about 90% of that of sucrose, and it has moisturizing properties that can improve food texture and extend shelf life [1]
- Regulatory Background: This assessment was conducted by the Food Standards Australia New Zealand (FSANZ) to update the energy value of maltitol in the Codex Alimentarius, ensuring that the energy content labeling of food is accurate so that consumers can obtain information and manage their diets [1]

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.)