Lactobacillus reuteri JCM 1112 ameliorates chronic acrylamide-induced glucose metabolism disorder via the bile acid-TGR5-GLP-1 axis and modulates intestinal oxidative stress in mice.

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  • Additional Information
    • Source:
      Publisher: Royal Society of Chemistry Country of Publication: England NLM ID: 101549033 Publication Model: Electronic Cited Medium: Internet ISSN: 2042-650X (Electronic) Linking ISSN: 20426496 NLM ISO Abbreviation: Food Funct Subsets: MEDLINE
    • Publication Information:
      Original Publication: Cambridge : Royal Society of Chemistry
    • Subject Terms:
      Acrylamide*/toxicity ; Bile Acids and Salts*/metabolism ; Glucagon-Like Peptide 1*/metabolism ; Limosilactobacillus reuteri* ; Oxidative Stress*/drug effects ; Probiotics*/pharmacology ; Receptors, G-Protein-Coupled*/metabolism ; Receptors, G-Protein-Coupled*/genetics; Animals ; Male ; Mice ; Blood Glucose/metabolism ; Glucagon-Like Peptides/pharmacology ; Insulin/metabolism ; Mice, Inbred C57BL
    • Abstract:
      Acrylamide (AA) is a toxic food contaminant that has been reported to cause glucose metabolism disorders (GMD) at high doses. However, it is unclear whether chronic low-dose AA can induce GMD and whether probiotics can alleviate AA-induced GMD. Here, C57BL/6N mice were orally administered with 5 mg per kg bw AA for 10 weeks, followed by another 3 weeks of glucagon-like peptide-1 (GLP-1) analogue (dulaglutide) treatment. Chronic low-dose AA exposure increased the blood glucose level and decreased serum insulin and GLP-1 levels, whereas dulaglutide treatment decreased the blood glucose level and increased the serum insulin level in AA-exposed mice. Then, mice were administered with AA or AA + INT-777 (Takeda G-protein-coupled receptor 5 (TGR5) agonist) for 10 weeks. INT-777 treatment reversed AA-induced downregulation of ileal TGR5 and proglucagon (PG) gene expression and decreased the serum GLP-1 level. These findings indicated that chronic low-dose AA induced GMD via inhibiting the TGR5-GLP-1 axis. Finally, mice were administered with AA for 10 weeks, followed by another 3 weeks of Lactobacillus reuteri JCM 1112 supplementation. L. reuteri supplementation significantly increased serum glucose, insulin and GLP-1 levels, upregulated ileal TGR5 and PG gene expression, and effectively restored the imbalance of bile acid (BA) metabolism in AA-exposed mice, demonstrating that L. reuteri ameliorates chronic AA-induced GMD via the BA-TGR5-GLP-1 axis. In addition, L. reuteri significantly enhanced ileal superoxide dismutase and catalase activities and total antioxidant capacity, thereby preventing chronic AA-induced oxidative stress. Our research provides new insights into the GMD toxicity of chronic low-dose AA and confirms the role of probiotics in alleviating AA-induced GMD.
    • Accession Number:
      20R035KLCI (Acrylamide)
      0 (Bile Acids and Salts)
      0 (Blood Glucose)
      89750-14-1 (Glucagon-Like Peptide 1)
      62340-29-8 (Glucagon-Like Peptides)
      0 (Gpbar1 protein, mouse)
      0 (Insulin)
      0 (Receptors, G-Protein-Coupled)
    • Publication Date:
      Date Created: 20240528 Date Completed: 20240617 Latest Revision: 20240716
    • Publication Date:
      20240717
    • Accession Number:
      10.1039/d4fo01061b
    • Accession Number:
      38804210