Abstract

Bile acids (BAs) are known to be involved in cholesterol metabolism but interactions between the diet, BA profiles, gut microbiota and lipid metabolism have not been extensively explored. In the present study, primary and secondary BAs including their glycine and taurine-conjugated forms were quantified in serum of Apoe−/− mice by protein precipitation followed by reversed phase ultra-high-performance liquid chromatography and QTOF mass spectrometry. The mice were fed different lingonberry fractions (whole, insoluble and soluble) in a high-fat setting or cellulose in a high and low-fat setting. Serum concentrations of BAs in mice fed cellulose were higher with the high-fat diet compared to the low-fat diet (20–70%). Among the lingonberry diets, the diet containing whole lingonberries had the highest concentration of chenodeoxycholic acid (CDCA), ursodeoxycholic acid (UDCA), tauro-ursodeoxycholic acid (T-UDCA), α and ω-muricholic acids (MCA) and tauro-α-MCA (T-α-MCA), and the lowest concentration of tauro-cholic acid (T-CA), deoxycholic acid (DCA) and tauro-deoxycholic acid (T-DCA). The glycine-conjugated BAs were very similar with all diets. CDCA, UDCA and α-MCA correlated positively with Bifidobacterium and Prevotella, and T-UDCA, T-α-MCA and ω-MCA with Bacteroides and Parabacteroides.

Highlights

  • Bile acids (BAs) are synthesized from cholesterol in the liver and stored in the gallbladder to be secreted in the duodenal lumen upon food intake in order to facilitate fat digestion

  • The increase was to a certain extent reflected in the group fed the insoluble lingonberry fraction, which was significant for β-muricholic acid (MCA) and chenodeoxycholic acid (CDCA) (P < 0.01)

  • The aim of the present study was to investigate the applicability of an UHPLC-MS method for determination of serum BAs in Apoe−/− mice fed diets containing different lingonberry materials, and whether the BA profile was related to gut microbiota composition

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Summary

Introduction

Bile acids (BAs) are synthesized from cholesterol in the liver and stored in the gallbladder to be secreted in the duodenal lumen upon food intake in order to facilitate fat digestion. Part of the secondary BAs is reabsorbed into the liver, conjugated and transported into the circulation. This means that changes in the colonic BA profile caused by diet may be reflected in blood. Up to 90% of the primary BAs in human adults are produced through the classical neutral pathway in the liver, while the remaining 10% are synthesized via the acidic pathway[9,10,11]. The BA pool size is kept comparatively stable at about 3–5 g through the enterohepatic circulation[14] In this process about 95% of the BAs that have entered the small intestine are reabsorbed from the terminal ileum back to the liver via the portal vein. There is a growing need for methods to identify and quantify BAs in biological matrices

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