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Long‐term drench of exopolysaccharide from Leuconostoc pseudomesenteroides XG5 protects against type 1 diabetes of NOD mice via stimulating GLP‐1 secretion.

Authors :
Pan, Lei
Xu, Min
Wang, Qi
Zou, Xuan
Han, Ye
Zhou, Zhijiang
Source :
Journal of the Science of Food & Agriculture; 3/30/2022, Vol. 102 Issue 5, p2023-2031, 9p
Publication Year :
2022

Abstract

BACKGROUND Type 1 diabetes is an autoimmune disease that results in the specific destruction of insulin‐producing beta cells in the pancreas. The aim of this study was to investigate the mechanism of exopolysaccharide from Leuconostoc pseudomesenteroides XG5 (XG5 EPS) against type 1 diabetes. RESULTS: Long‐term drench of XG5 EPS delayed the onset of autoimmune diabetes and had fewer islets with high‐grade infiltration (an insulitis score of 3 or 4) than untreated NOD mice. Oral administration of 50 mg kg−1 d−1 XG5 EPS increased the insulin and glucagon‐like peptide‐1 (GLP‐1) levels of serum, stimulated GLP‐1 secretion and upregulated gcg mRNA expression of colon in NOD mice. Moreover, oral administration of 50 mg kg−1 d−1 XG5 EPS significantly increased total short‐chain fatty acids levels in the colon contents, especially those of acetic acid and butyric acid. In NCI‐H716 cells, 500 and 1000 μmol L−1 sodium butyrate promoted the secretion of GLP‐1 and upregulated the mRNA expression of gcg and PC3, while XG5 EPS and sodium acetate did not stimulate the GLP‐1 secretion. Therefore, long‐term drench of XG5 EPS delayed the onset of autoimmune diabetes, which may be directly correlated with the increase of butyrate in the colon of NOD mice. CONCLUSION: Long‐term drench of 50 mg kg−1 d−1 XG5 EPS promoted the expression and secretion of GLP‐1 by increasing the production of butyric acid, thereby delaying T1D onset in NOD mice. © 2021 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00225142
Volume :
102
Issue :
5
Database :
Complementary Index
Journal :
Journal of the Science of Food & Agriculture
Publication Type :
Academic Journal
Accession number :
155662731
Full Text :
https://doi.org/10.1002/jsfa.11541