Acrylamide induced glucose metabolism disorder in rats involves gut microbiota dysbiosis and changed bile acids metabolism. (July 2022)

• Record Type: Journal Article
• Authors: Yue, Zonghao; Chen, Yanjuan; Dong, Qian; Li, Dan; Guo, Meng; Zhang, Li; Shi, Yini; Wu, Huiting; Li, Lili; Sun, Zhongke
• Is Part Of: Food research international. Volume 157(2022)
• Publication Date: 2022-07
• Subjects: Acrylamide -- Glucose metabolism disorder -- Gut microbiota -- Bile acids -- Farnesoid X receptor -- Glucagon-like peptide-1; Food -- Analysis -- Periodicals; Food industry and trade -- Periodicals; Food industry and trade -- Canada -- Periodicals; Food Technology -- Periodicals; Food -- Periodicals; Food-Processing Industry -- Periodicals; Aliments -- Industrie et commerce -- Périodiques; Aliments -- Industrie et commerce -- Canada -- Périodiques; Aliments -- Recherche -- Périodiques; Food industry and trade; Canada; Periodicals; Electronic journals; 664.005
• DOI: 10.1016/j.foodres.2022.111405
• Languages: English
• ISSNs: 0963-9969

Abstract

Graphical abstract: Highlights: Acrylamide (AA) increased glucose level and decreased insulin level. AA caused intestinal barrier injury in ileum. AA led to gut microbiota (GM) imbalance and bile acids (BAs) metabolic alternation. GM-BAs-FXR/GLP-1 pathway contributed greatly to AA-induced gut metabolism disorder. Abstract: Acrylamide (AA) is a common food contaminant that causes glucose metabolism disorders (GMD). However, the underlying mechanism remains unclear. Female Sprague Dawley (SD) rats were treated with AA via gavage for 21 days, and the glucose and insulin levels, gut microbiota, intestinal barrier, and metabolism were analyzed. The results revealed that AA elevated serum glucose levels, reduced insulin levels and caused intestinal barrier injury. The 16S amplicon sequencing and non-targeted metabolomics showed that AA induced gut microbiota dysbiosis and bile acids (BAs) metabolism disorder. Specifically, AA decreased the abundance of Lactobacillus and Bacteroides in the cecal contents, and increased the cholic acid (CA) content in feces. Meanwhile, the expression of ileum apical sodium-dependent bile acid transporter (ASBT) responsible for CA reabsorption was suppressed. Further analysis indicated that BAs sensing nuclear receptor farnesoid X receptor (FXR) gene was activated and glucagon-like peptide-1 (GLP-1) which stimulates insulin secretion was downregulated. In addition, activation of FXR increased the expression of fibroblast growth factor 15 (FGF15), which resulted in the inhibition of hepatic BAs synthesis. Overall, this study demonstrated that AA-induced GMD is associated with the gut-microbiota-CA-FXR/GLP-1 axis. These findings add new knowledge to the AA-induced GMD and provide a basis for potential AA toxicity mitigation by manipulation of the gut microbiota.