Bile Acid

Bile acid compounds can be divided into free and conjugated bile acids, or primary and secondary. With our own bile acid database, MetwareBio offers absolute quantification of 65 molecules in a single run.

Technology Introduction

24-carbon sterols, also known as bile acids, are synthesized in the liver from cholesterol and are the primary components of the bile. These alkanoic acids play a crucial role in regulating metabolism by maintaining cholesterol balance and promoting lipid digestion and absorption. They also possess anti-inflammatory and antiseptic properties. While most bile acids are recycled through hepatic and intestinal circulation, around 5% are eventually excreted in feces.


Product superiority of Bile Acid Service

  • Absolute quantification: 65 standard curves, r > 0.99, 13 isotope internal standards;
  • High sensitivity: AB QTRAP® 6500+ LC-MS/MS,ng/ml concentration can be detected;
  • Wide coverage: Large number of important bile acids in the panel.

Application Direction

Biomaker screening
Screen for differential bile acids, establish diagnostic markers and validation models.
Functional Studies
Linking differential bile acids to observed phenotype.
Mechanism research
Understand mode of action through pathway analysis and combining with other Omics data.

Bile acids Targeted Metabolism Test Services Case Study

Article Spotlight:  Intrahepatic cholestasis induced by α-naphthylisothiocyanate can cause gut-liver axis disorders


Clinical studies have shown that Intrahepatic cholestasis is closely related to intestinal injury. The gut-liver axis theory suggests that the intestine and liver are closely related, and that bile acids are important mediators linking the intestine and liver. We compared two cholestasis models: a single injection model that received a single subcutaneous ANIT injection (75 mg/kg), and a multiple subcutaneous injection model that received an injection of ANIT (50 mg/kg) every other day for 2 weeks. We used Transmetil (ademetionine 1,4-butanedisulfonate) to relieve intrahepatic cholestasis in the multiple injection group. In the multiple injection group, we found increased hepatic bile duct hyperplasia, increased fibrosis of the liver, increased small intestine inflammation and oxidative damage, increased harmful bile acids, decreased bile acids transporter levels. After treatment with Transmetil, the liver and gut injuries were relieved. These results suggest that intrahepatic cholestasis can cause disorders of the gut-liver axis.


Article Spotlight: QiDiTangShen granules modulated the gut microbiome composition and improved bile acid profiles in a mouse model of diabetic nephropathy

Article Spotlight:  Runt-related transcription factor-1 ameliorates bile acid-induced hepatic inflammation in cholestasis through JAK/STAT3 signaling

Background and aims: Bile acids trigger a hepatic inflammatory response, causing cholestatic liver injury. Runt-related transcription factor-1 (RUNX1), primarily known as a master modulator in hematopoiesis, plays a pivotal role in mediating inflammatory responses. However, RUNX1 in hepatocytes is poorly characterized, and its role in cholestasis is unclear. Herein, we aimed to investigate the role of hepatic RUNX1 and its underlying mechanisms in cholestasis.

Approach and results: Hepatic expression of RUNX1 was examined in cholestatic patients and mouse models. Mice with liver-specific ablation of Runx1 were generated. Bile duct ligation and 1% cholic acid diet were used to induce cholestasis in mice. Primary mouse hepatocytes and the human hepatoma PLC/RPF/5- ASBT cell line were used for mechanistic studies. Hepatic RUNX1 mRNA and protein levels were markedly increased in cholestatic patients and mice. Liver-specific deletion of Runx1 aggravated inflammation and liver injury in cholestatic mice induced by bile duct ligation or 1% cholic acid feeding. Mechanistic studies indicated that elevated bile acids stimulated RUNX1 expression by activating the RUNX1 -P2 promoter through JAK/STAT3 signaling. Increased RUNX1 is directly bound to the promotor region of inflammatory chemokines, including CCL2 and CXCL2 , and transcriptionally repressed their expression in hepatocytes, leading to attenuation of liver inflammatory response. Blocking the JAK signaling or STAT3 phosphorylation completely abolished RUNX1 repression of bile acid-induced CCL2 and CXCL2 in hepatocytes.

Conclusions: This study has gained initial evidence establishing the functional role of hepatocyte RUNX1 in alleviating liver inflammation during cholestasis through JAK/STAT3 signaling. Modulating hepatic RUNX1 activity could be a new therapeutic target for cholestasis.

List of Metabolites

Index Compounds CAS Abbreviation
1 taurolithocholic acid-3-sulfate 15324-65-9 TLCA-3S
2 Dehydrolithocholic acid 1553-56-6 DLCA
3 Isoallolithocholic acid 2276-93-9 IALCA
4 Lithocholic acid 434-13-9 LCA
5 isolithocholic acid 1534-35-6 ILCA
6 Nor-Deoxycholic Acid 53608-86-9 23-DCA
7 3-oxodeoxycholic acid 4185-01-7 3-oxo-DCA
8 7-ketolithocholic acid 4651-67-6 7-KLCA
9 12-ketolithocholic acid 5130-29-0 12-KLCA
10 murideoxycholic acid 668-49-5 MDCA
11 Deoxycholic acid 83-44-3 DCA
12 Isodeoxycholic acid 566-17-6 IDCA
13 3β-deoxycholic acid 570-63-8 3β-DCA
14 3β-Ursodeoxycholic Acid 78919-26-3 3β-UDCA
15 Ursodeoxycholic acid 128-13-2 UDCA
16 β-Hyodeoxycholic Acid 570-84-3 3β-HDCA
17 Hyodeoxycholic acid 83-49-8 HDCA
18 Chenodeoxycholic acid 474-25-9 CDCA
19 norcholic acid 60696-62-0 NCA
20 Dehydrocholic acid 81-23-2 DHCA

Project Workflowe

Sample Requirements of Bile Acid

Sample Type Sample Recommended
Minimum Sample Biological
Liquid Plasma, serum, hemolymph, bile 100μL 20μL

Tissue Animal tissue, placenta, thrombus 100mg 20mg
Feces Feces, ilntestinal contents 200 mg
(wet weight)
50 mg
(wet weight)


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