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.
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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DOI:
10.3389/fnut.2021.769341
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发表时间:
2021
影响因子:
5
通讯作者:
Vasu C
中科院分区:
文献类型:
--
作者:
Taylor HB;Vasu C
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.
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影响因子:
11.1
作者:
Jian C;Carpén N;Helve O;de Vos WM;Korpela K;Salonen A
通讯作者:
Salonen A
影响因子:
4.2
作者:
Gudi, Radhika;Suber, Jada;Vasu, Chenthamarakshan
通讯作者:
Vasu, Chenthamarakshan
影响因子:
64.5
作者:
Chung H;Pamp SJ;Hill JA;Surana NK;Edelman SM;Troy EB;Reading NC;Villablanca EJ;Wang S;Mora JR;Umesaki Y;Mathis D;Benoist C;Relman DA;Kasper DL
通讯作者:
Kasper DL
影响因子:
6.1
作者:
Liu, Bo;Lin, Qinlu;Luo, Feijun
通讯作者:
Luo, Feijun
DOI:
10.1111/j.2517-6161.1995.tb02031.x
发表时间:
1995-01-01
影响因子:
5.8
作者:
BENJAMINI, Y;HOCHBERG, Y
通讯作者:
HOCHBERG, Y