Biological Mechanisms of Aflatoxin B<sub>1</sub>-Induced Bile Metabolism Abnormalities in Ducklings

This study investigated the effects and biological mechanisms of aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) on the health and bile metabolism of ducklings. Forty-eight 1-day-old ducklings were randomly assigned to two groups, with six replicates per group. The control group wa...

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Bibliographic Details
Main Authors: Yihong Chu, Aimei Yu, Huanbin Wang, Shahid Ali Rajput, Qianqian Yu, Desheng Qi
Format: Article
Language:English
Published: MDPI AG 2024-10-01
Series:Animals
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Online Access:https://www.mdpi.com/2076-2615/14/20/2996
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Summary:This study investigated the effects and biological mechanisms of aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) on the health and bile metabolism of ducklings. Forty-eight 1-day-old ducklings were randomly assigned to two groups, with six replicates per group. The control group was fed a basic diet, while the AFB<sub>1</sub> group received a diet containing 90 µg/kg of AFB<sub>1</sub>. The experiment lasted for 2 weeks. The results showed that 90 µg/kg AFB<sub>1</sub> caused abnormal bile metabolism; damaged liver cell nuclei and mitochondria; and significantly decreased body weight, average daily weight gain, and levels of albumin, total protein, cholesterol, total superoxide dismutase, glutathione peroxidase, and glutathione. It also significantly increased feed conversion efficiency, along with alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total bile acids, and malondialdehyde levels. In the liver, the expression levels of <i>CYP7A1</i>, <i>SCD</i>, and other genes were significantly upregulated, while <i>BSEP</i>, <i>FASN</i>, <i>HMGCR</i>, <i>CAT</i>, and other genes were significantly downregulated. In conclusion, AFB<sub>1</sub> causes abnormal bile metabolism and impairs the overall health and liver function of ducklings. Its mechanism of action may involve changes in gene expression related to bile acid metabolism, lipid metabolism, oxidative damage, and cancer pathways.
ISSN:2076-2615