2. Academic Validation
  3. Turnover of bile acids in liver, serum and caecal content by high-fat diet feeding affects hepatic steatosis in rats

Turnover of bile acids in liver, serum and caecal content by high-fat diet feeding affects hepatic steatosis in rats

  • Biochim Biophys Acta Mol Cell Biol Lipids. 2019 Oct;1864(10):1293-1304. doi: 10.1016/j.bbalip.2019.05.016.
Yingyue Tang 1,  Jingyi Zhang 1,  Jing Li 1,  Xiaohong Lei 1,  Dongke Xu 2,  Yang Wang 3,  Chunmin Li 1,  Xiaobo Li 4,  Yimin Mao 5
Affiliations

Affiliations

  • 1 Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
  • 2 Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
  • 3 Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  • 4 Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China. Electronic address: [email protected].
  • 5 Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Electronic address: [email protected].
PMID: 31170503 DOI: 10.1016/j.bbalip.2019.05.016
Abstract

Background: Bile acids (BAs) participate in lipid absorption and serve as metabolic regulatory factors in gut-liver communication. To date, there are no studies on the systemic patterns of BAs in the serum, liver, and gut in the same non-alcoholic fatty liver disease (NAFLD) model.

Methods: A targeted metabolomics approach and 16S rRNA sequencing were used to identify the profile of BAs and connection between BAs and microbiota. The role and mechanism of altered BAs on hepatic steatosis were investigated.

Findings: In the liver, the composition of taurocholic acid (TCA) was increased, but taurohyodeoxycholic acid (THDCA) and ursodeoxycholic acid (UDCA) were decreased. In the gut, the deconjugated form of TCA (cholic acid (CA)) was increased, while the deconjugated forms of THDCA (α-hyodeoxycholic acid (HDCA)) and ω-muricholic acid (ωMCA) were decreased. In the serum, the composition of TCA was increased, while both HDCA and THDCA were decreased. THDCA induced the gene expression of apolipoprotein, bile secretion-related proteins, and Cytochrome P450 family but suppressed inflammatory response genes expression in steatotic hepatocytes by RNAseq analysis. THDCA ameliorated neutral lipid accumulation and improved Insulin sensitivity in primary rat hepatocytes. The decreased HDCA level correlated with the level of Bacteroidetes, while the level of CA correlated with the levels of Firmicutes and Verrucomicrobia but correlated inversely with Bacteroidetes.

Conclusion: BAs profiles in the serum, liver and caecal content were altered in a rat NAFLD model, which may affect hepatic lipid accumulation and correlate with gut dysbiosis.

Keywords

Bile acid; Gut microbiota; Non-alcoholic fatty liver disease; TCA; THDCA.

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