Co-exposure to different bacterial species' lipopolysaccharides with the NASH diet exacerbates NASH and liver fibrosis progression in mice.
Journal
Clinics and research in hepatology and gastroenterology
Journal Volume
48
Journal Issue
9
Pages
02470
ISSN
2210-741X
Date Issued
2024-11
Author(s)
Lee, Yen-Peng
Chiu, Chien-Chao
Chang, Yung-Chi
Chen, Yi-Hsun
Chuang, Hsiao-Li
Abstract
With the obesity epidemic, nonalcoholic fatty liver disease (NAFLD) has become a public health concern, but its progression mechanism remains unclear. Experimental models mimicking human NAFLD/steatohepatitis (NASH) are crucial. This study simulates gut microbiota imbalance effects on NASH and liver fibrosis.
We used different bacterial sources of lipopolysaccharide (LPS), including Escherichia coli (GEC) and Salmonella abortus equi (GSE), combined with a Gubra Amylin NASH (GAN) diet to induce NASH and liver fibrosis.
The GSE group showed significantly higher serum alanine aminotransferase, hydroxyproline, CD68-positive cells, α-smooth muscle actin, glial fibrillary acidic protein, and TNF-α, COL1A1, TGF-β, and NLRP3 expressions compared to the the GAN group. The GSE group also had higher Erysipelotrichaceae, Akkermansiaceae, and Bacteroidaceae family numbers.
The GAN diet with LPS treatment successfully induced NASH and fibrosis making this model useful for preclinical NASH drug testing.
Subjects
Fibrosis
Gut microbiota
Hepatic inflammatory
LPS
Nonalcoholic steatohepatitis
Type
journal article