Manganese Chloride Attenuates Gut Dysmotility, Dysbiosis, and Ileal Bile Acid Malabsorption during Diabetes-Induced Cholesterol Gallstone in Swiss Mice
DOI:
https://doi.org/10.4314/Từ khóa:
Cholesterol gallstone, manganese chloride, small intestinal motility, gut dysbiosis, ileum bile acids malabsorptionTóm tắt
Background: Accumulation of bile acids (BA) from intestinal BA malabsorption causes gut dysmotility, leading to gut dysbiosis, which is evident in obesity and diabetes mellitus. Diabetes mellitus has been reported to facilitate progression of Cholesterol Gallstone (CGS) pathogenesis in patients.
Objectives: Manganese Chloride (MnCl2) attenuates CGS formation but there is paucity of information regarding its activities on BA malabsorption during CGS formation in diabetic Swiss mice, which this study design investigated
Materials and Methods: One hundred and forty female Swiss mice (n=20) were grouped into 7: I-normal control, II-untreated CGS, III-normal+0.37 mg/kg or IV-normal+0.74 mg/kg MnCl2, 5-CGS+0.37 mg/kg or VI-CGS+0.74 mg/kg MnCl2, and VII-CGS+75mg/kg aspirin. Alloxan-induced diabetic mice were fed with cholesterol-rich diets to induce CGS. Blood glucose level (BGL) was monitored and intestinal motility, fecal cholesterol, BA, biochemical analysis of excised ileum, total bacterial load of ileum homogenate and stool samples, ileum histopathology and morphometric evaluations were determined at 2 and 4-weeks. Data was analyzed using ANOVA, expressed as Mean±SEM and significant at p≤0.05.
Results: Weekly BGL significantly decreased in CGS+MnCl2 groups. Intestinal motility significantly increased in normal and CGS+0.37mg/kg MnCl2 compared with untreated CGS groups at 2 and 4-weeks. Intestinal malondialdehyde, mast cell counts, and fecal BA levels were significantly decreased while nitric-oxide, mucin level, Na+/K+-ATPase activity, villi/crypt, villi absorption area and commensal bacteria were increased in CGS+MnCl2 compared with untreated CGS groups at 2 and 4-weeks.
Conclusion: Manganese chloride attenuated diabetic induced cholesterol gallstone gut dysmotility through stimulated bile acid absorption, reduced intestinal mast cell count and pathogenic gut bacteria.
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