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. 2022 Oct 19:5:1976-1984.
doi: 10.1016/j.crfs.2022.10.021. eCollection 2022.

Dietary acetic acid suppress high-fat diet-induced obesity in mice by altering taurine conjugated bile acids metabolism

Rui Wang  1 , Xiuqin Fan  1 , Yuanyuan Lu  2 , Dawei Chen  3 , Yunfeng Zhao  3 , Kemin Qi  1
Affiliations

Dietary acetic acid suppress high-fat diet-induced obesity in mice by altering taurine conjugated bile acids metabolism

Rui Wang et al. Curr Res Food Sci. .

Abstract

Vinegar is widely used in Chinese diet as a traditional condiment, and its functional component acetic acid has been proposed to prevent obesity, while its mechanism is still unclear. Bile acids (BAs) have been reported to have a protective effect on obesity. This study demonstrated that high-fat diet induced obesity (DIO) seriously disturbed BAs balance by significantly decreasing hepatic BAs synthesis and increasing fecal BAs excretion. However, acetate supplemented in the high-fat diet can restore BAs balance by mainly promoting hepatic taurine conjugated BAs (tauro-BAs) synthesis and decreasing fecal tauro-BAs excretion. The tauro-BAs, as the antagonists, inhibited the intestinal-liver farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15)-FGF receptor 4 (FGFR4) signaling pathway, and negatively regulated the production of hepatic BAs. Present study provided important clues for further investigation of the mechanism of acetic acid inhibiting DIO.

Keywords: Acetic acid; Antagonist; Bile acids; FXR; Obesity.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Image 1
Graphical abstract
Fig. 1
Fig. 1
Effects of acetate on body weight and metabolic indicators in mouse serum and liver. Note: d: the sum of the subcutaneous and epididymal fat; e: the body fat ratio, 100% * (subcutaneous fat weight + epididymal fat weight)/body weight; g: the liver index, 100% * liver weight/body weight; * Compared to the C group; # compared to the HFD group. p < 0.05 (*/#), p < 0.01 (**/##), p < 0.001 (***/###).
Fig. 2
Fig. 2
SCFAs concentrations of mouse feces, serum and liver. Note: * Compared to the C group; # compared to the HFD group. p < 0.05 (*/#), p < 0.01 (**/##), p < 0.001 (***/###).
Fig. 3
Fig. 3
BAs concentrations and percentages in mouse liver, serum and feces. Note: b, c, d: BAs percentages in mouse liver; f, g, h: BAs percentages in mouse serum; j, k, l: BAs percentages in mouse feces. TDCA: taurodeoxycholic acid, 7-DCA: 7-dehydrocholic acid, 3-DCA: 3-dehydrocholic acid, muroCA: murocholic acid, HCA: hyocholic acid, NorDCA: nordeoxycholic acid, UCA: ursocholic acid, apoCA: apocholic acid, 7-DHCA: 7-dehydrocholic acid, 3-DHCA: 3-dehydrocholic acid, 12-DHCA: 12-dehydrocholic acid. * Compared to the C group; # compared to the HFD group. p < 0.05 (*/#), p < 0.01 (**/##), p < 0.001 (***/###).
Fig. 4
Fig. 4
Effects of acetate on the mRNA expression of hepatic and ileal related enzymes and transporters that involve in cholesterol and BAs metabolism. The expression of genes associated with BAs synthesis (CYP7A1, CYP8B1 and CYP27A1), negative feedback regulation of BAs synthesis (FXR, SHP and FGFR4), and cholesterol synthesis and secretion (HMGR and ABCG5) in the hepatic tissue (a–h). The expression of genes associated with negative feedback regulation of BAs synthesis (FXR and FGF15), BAs reabsorption (ASBT) and cholesterol secretion (ABCG5) in the ileum(i-l). * Compared to the C group; # compared to the HFD group. p < 0.05 (*/#), p < 0.01 (**/##), p < 0.001 (***/###).
Fig. 5
Fig. 5
FXR negatively feedback regulation of BAs synthesis. Hepatic cholesterol results from HMGR mediated conversion of acetate. BAs are synthesized from cholesterol by a series of enzymes including the initial and rate-limiting CYP7A1 in hepatocytes. BAs bind to FXR in the nucleus. In hepatocytes, FXR induces SHP, which inhibits transcription of CYP7A1 and BAs synthesis. Intestinal FXR induces FGF15, which circulates to the liver and binds to hepatic FGFR4, inhibiting transcription of CYP7A1 and BAs synthesis. ASBT expressed in the brush border of terminal ileal enterocytes mediate approximately 95% of BAs reabsorption. ABCG5/8 secretes cholesterol from hepatocytes into the bile. The cholesterol is transferred to the brush border membrane of enterocytes via bile salt micelles. Then, ABCG5/8 mediates biliary and cholesterol from the brush border membrane back into the gut lumen for excretion.
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