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Impact of Prebiotic β-glucan Treatment at Juvenile Age on the Gut Microbiota Composition and the Eventual Type 1 Diabetes Onset in Non-obese Diabetic Mice.

ABSTRACT: Complex dietary polysaccharides such as β-glucans are widely used for their anti-inflammatory properties. We reported before that oral administration of Yeast β-glucan (YBG) in adult mice can help delay type 1 diabetes (T1D) onset and suppress gut inflammation through modulation of the structure and function of gut microbiota. Since juvenile age is characterized by profoundly changing immature gut microbiota, we examined the impact of oral treatment with YBG in non-obese diabetic (NOD) mice at this age. Juvenile mice that received daily oral administration of YBG starting at 15 days of age for 7 or 30 days were examined for changes in gut microbiota, immune characteristics, and T1D incidence. Mice that received YBG for 30 days but not 7 days, showed considerable changes in the composition and diversity of fecal microbiota as compared to controls. Predictive functional analysis, based on 16S rDNA sequences, revealed overrepresentation of glycan biosynthesis and metabolism, energy metabolism, and fatty acid biosynthesis pathways in mice that received YBG for 30 days. Immune phenotype of the colon showed skewing toward immune regulatory and Th17 cytokines with increases in IL-10, IL-17, and IL-21 and a decrease in TNF-α, although increases in some pro-inflammatory cytokines (IL-1b, IFN-γ) were observed. Most importantly, mice that received YBG treatment for 30 days showed significantly suppressed insulitis and delayed onset of hyperglycemia compared to controls. Overall, this study suggests that oral consumption of YBG beginning at pre-diabetic juvenile ages could have positive maturational changes to gut microbiota and immune functions and could result in a delay in the disease onset in those who are pre-disposed to T1D.

SUBMITTER: Taylor HB

PROVIDER: S-EPMC8595985 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Recent evidence suggests there is a link between metabolic diseases and gut microbiota. To investigate the gut microbiota composition and fecal metabolic phenotype in diabetic retinopathy (DR) patients. DNA was extracted from 50 fecal samples (21 individuals with type 2 diabetes mellitus-associated retinopathy (DR), 14 with type 2 diabetes mellitus but without retinopathy (DM) and 15 sex- and age-matched healthy controls) and then sequenced by high-throughput 16S rDNA analysis. Liquid chromatography mass spectrometry (LC-MS)-based metabolomics was simultaneously performed on the samples. A significant difference in the gut microbiota composition was observed between the DR and healthy groups and between the DR and DM groups. At the genus level, Faecalibacterium, Roseburia, Lachnospira and Romboutsia were enriched in DR patients compared to healthy individuals, while Akkermansia was depleted. Compared to those in the DM patient group, five genera, including Prevotella, were enriched, and Bacillus, Veillonella, and Pantoea were depleted in DR patients. Fecal metabolites in DR patients significantly differed from those in the healthy population and DM patients. The levels of carnosine, succinate, nicotinic acid and niacinamide were significantly lower in DR patients than in healthy controls. Compared to those in DM patients, nine metabolites were enriched, and six were depleted in DR patients. KEGG annotation revealed 17 pathways with differentially abundant metabolites between DR patients and healthy controls, and only two pathways with differentially abundant metabolites were identified between DR and DM patients, namely, the arginine-proline and α-linolenic acid metabolic pathways. In a correlation analysis, armillaramide was found to be negatively associated with Prevotella and Subdoligranulum and positively associated with Bacillus. Traumatic acid was negatively correlated with Bacillus. Our study identified differential gut microbiota compositions and characteristic fecal metabolic phenotypes in DR patients compared with those in the healthy population and DM patients. Additionally, the gut microbiota composition and fecal metabolic phenotype were relevant. We speculated that the gut microbiota in DR patients may cause alterations in fecal metabolites, which may contribute to disease progression, providing a new direction for understanding DR.

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Impact of Prebiotic β-glucan Treatment at Juvenile Age on the Gut Microbiota Composition and the Eventual Type 1 Diabetes Onset in Non-obese Diabetic Mice.

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