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Effects of Long-Term Feeding of Dietary Allitol on Glucose Tolerance and Fecal Microbiota Profiles in Rats

DOI: 10.4236/jbm.2025.135006, PP. 59-74

Keywords: Allitol, Butyric Acid, Glucose Tolerance, Fecal Microbiota, Rat

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Abstract:

This study aimed to investigate the effect of long-term feeding of dietary allitol on glucose tolerance and the fecal microbiota profile in rats. The basic data was obtained, and the production of butyric acid from allitol was predicted using bioinformatic techniques. Furthermore, this study examined whether the anti-diabetic effect of allitol was due to gut microbiota. Fifty male Wistar rats, aged 4 weeks, were randomly divided into two groups of 25: control (C) and allitol (A). They were fed a commercial diet containing 3% sucrose or allitol. After feeding them for 16 weeks, oral and intraperitoneal glucose tolerance tests (OGTT and IPGTT, respectively) chowed that blood glucose levels before and after glucose administration were lower in Group A than in Group C. The area under the curve (AUC) was also lower in Group A than in Group C. After 24 weeks of the feeding period, Plasma glucose, insulin, and triglyceride concentrations and HOMA-R values were significantly lower in Group A than in Group C. Taxonomic changes in the microbial communities were assessed at the genus level. Changes in the microbiota indicated a significant increase in the abundance of the genera Blautia, Anaerostipes, and Acetitomaculum, known butyric acid producers. Potential differences in the function of the microbial community were evaluated using the PICRUSt2. Regarding butyric acid metabolism-related enzymes, butyryl-CoA: acetate-CoA transferase, trans-2-enoyl-CoA reductase (NAD+), butyrate kinase, and butanol dehydrogenase were significantly higher in Group A than in Group C. These results suggest that several compositional changes in the fecal microbiota and an increase in predicted butyric acid metabolism following dietary allitol supplementation. The anti-diabetic effect of allitol was confirmed; however, it was suggested that there may be other causes of this effect besides butyric acid produced by intestinal microbiota.

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