Taurohyocholic Acid
(Synonyms: 牛磺胆酸,Tauro-γ-muricholic Acid) 目录号 : GC45574Taurohyocholic Acid是一种由猪胆酸衍生的结合牛磺酸的胆汁酸，主要存在于猪胆汁中。
Cas No.:32747-07-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
Cell lines | STC-1 |
Preparation Method | The STC-1 cell were plated into 24 well-plates with an initial cell density of 2*105 cells/well, treated with 25µM Taurohyocholic Acid for 1h. The cell media was removed from the cells, centrifuged at 2,000g for 10min to remove cell debris and the supernatant was collected. An GLP-1 ELISA kit was used to measure GLP-1. |
Reaction Conditions | 25µM, 1h |
Applications | Taurohyocholic Acid can upregulated GLP-1 secretion in STC-1 cells. |
References: | |
Taurohyocholic Acid is a taurine-conjugated bile acid derived from hyocholic acid, predominantly found in pig bile[1]. Taurohyocholic Acid plays a crucial role in glucose homeostasis[2] and metabolic regulation[3]. It is also used in research of oncology[4] and end-stage renal disease (ESRD)[5] as a biomarker for predicting treatment efficacy.
Taurohyocholic Acid stimulate GLP-1 production and secretion in intestinal enteroendocrine STC-1 and NCI-H716 cells by promoting proglucagon transcription. In STC-1 and NCI-H716 cells, treatment with 25µM Taurohyocholic Acid for 1 hour significantly increased GLP-1 secretion, and a 24-hour incubation further promoted proglucagon transcription and GLP-1 production[6].
References:
[1]. Fang W, Wen X, Meng Q, et al. Alteration in bile acids profile in Large White pigs during chronic heat exposure. J Therm Biol. 2019 Aug;84:375-383. doi: 10.1016/j.jtherbio.2019.07.027. Epub 2019 Jul 26. PMID: 31466777.
[2]. Cheng Z, Liu G, Zhang X, et al. Improvement of Glucose Metabolism Following Long-Term Taurocholic Acid Gavage in a Diabetic Rat Model. Med Sci Monit. 2018 Oct 9;24:7206-7212. doi: 10.12659/MSM.912429. PMID: 30298865; PMCID: PMC6192455.
[3]. Zheng X, Chen T, Zhao A, et al. Hyocholic acid species as novel biomarkers for metabolic disorders. Nat Commun. 2021 Mar 5;12(1):1487. doi: 10.1038/s41467-021-21744-w. PMID: 33674561; PMCID: PMC7935989.
[4]. Chen Y, Wang Y, Lei J, et al. Taurohyocholic acid acts as a potential predictor of the efficacy of tyrosine kinase inhibitors combined with programmed cell death-1 inhibitors in hepatocellular carcinoma. Front Pharmacol. 2024 Feb 23;15:1364924. doi: 10.3389/fphar.2024.1364924. PMID: 38464731; PMCID: PMC10920247.
[5]. Chen WY, Zhang JH, Chen LL, et al. Bioactive metabolites: a clue to the link between MASLD and CKD? Clin Mol Hepatol. 2024 Oct 21. doi: 10.3350/cmh.2024.0782. Epub ahead of print. PMID: 39428978.
[6]. Zheng X, Chen T, Jiang R, et al. Hyocholic acid species improve glucose homeostasis through a distinct TGR5 and FXR signaling mechanism. Cell Metab. 2021 Apr 6;33(4):791-803.e7. doi: 10.1016/j.cmet.2020.11.017. Epub 2020 Dec 17. PMID: 33338411.
Taurohyocholic Acid是一种由猪胆酸衍生的结合牛磺酸的胆汁酸，主要存在于猪胆汁中[1]。Taurohyocholic Acid在维持血糖稳态[2]和代谢调节[3]中起关键作用。在肿瘤学[4]和终末期肾病（ESRD）[5] 研究中，Taurohyocholic Acid可以作为预测治疗效果的生物标志物。
Taurohyocholic Acid可以通过促进前胰高血糖素转录，刺激STC-1和NCI-H716细胞中GLP-1的生成和分泌。在STC-1和NCI-H716细胞中，用25µM的Taurohyocholic Acid处理1小时可以显著增加GLP-1分泌，24小时的孵育进一步促进了前胰高血糖素转录和GLP-1的生成[6]。
| Cas No. | 32747-07-2 | SDF | |
| 别名 | 牛磺胆酸,Tauro-γ-muricholic Acid | ||
| 化学名 | 2-[[(3α,5β,6α,7α)-3,6,7-trihydroxy-24-oxocholan-24-yl]amino]-ethanesulfonic acid | ||
| Canonical SMILES | O[C@@H]1CC[C@@]2(C)[C@@]([C@@H](O)[C@@H](O)[C@]3([H])[C@]2([H])CC[C@@]4(C)[C@@]3([H])CC[C@]4([H])[C@H](C)CCC(NCCS(O)(=O)=O)=O)([H])C1 | ||
| 分子式 | C26H45NO7S | 分子量 | 515.7 |
| 溶解度 | 20mg/mL in ethanol, or DMSO, 30mg/mL in DMF | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.9391 mL | 9.6956 mL | 19.3911 mL |
| 5 mM | 0.3878 mL | 1.9391 mL | 3.8782 mL |
| 10 mM | 0.1939 mL | 0.9696 mL | 1.9391 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Targeted Metabolomics Reveals Birth Screening Biomarkers for Biliary Atresia in Dried Blood Spots
J Proteome Res 2022 Mar 4;21(3):721-726.PMID:34850627DOI:10.1021/acs.jproteome.1c00775.
Early diagnosis and timely surgical Kasai portoenterostomy greatly improve the survival of patients with biliary atresia (BA), a neonatal cholestatic disease, which has encouraged investigators to develop newborn screening for BA. In this study, we used ultraperformance liquid chromatography-triple quadrupole mass spectrometry-based targeted metabolomics profiling to identify potential BA biomarkers in dried blood spots (DBS) collected from BA patients (n = 21) and healthy controls (n = 100). A distinctive metabolic profile comprising eight significantly differentially expressed metabolites, Taurohyocholic Acid (THCA), glutamic acid, 2-hydroxyglutaric acid, ketoleucine, indoleacetic acid, alpha-ketoisovaleric acid, glycocholic acid, and taurocholic acid (TCA), clearly distinguished BA infants from control neonates. Three metabolites, THCA, 2-hydroxyglutaric acid, and indoleacetic acid, were selected using linear regression and receiver operating characteristic (ROC) curve analysis and model construction. The area under the ROC curve for this model to discriminate between BA and comparison infants was 0.938 (95% confidence interval, CI: 0.874-1.000). A cutoff value of -0.336 produced a sensitivity of 90.48% (95% CI: 69.62% - 98.83%) and specificity of 92% (95% CI: 84.84% - 96.48%). In conclusion, the results suggest that metabolic markers in DBS obtained from newborns have a great potential for BA screening.
Glucagon-Like Peptide-2 Alters Bile Acid Metabolism in Parenteral Nutrition--Associated Liver Disease
JPEN J Parenter Enteral Nutr 2016 Jan;40(1):22-35.PMID:26220199DOI:10.1177/0148607115595596.
Background: We aim to study the mechanisms underlying our previous finding that exogenous glucagon-like peptide-2 (GLP-2) treatment in a preclinical model of neonatal parenteral nutrition-associated liver disease (PNALD) improves cholestasis. Methods: Neonatal piglets received 17 days of parenteral nutrition (PN) therapy and either saline control (PN/Saline n = 8) or GLP-2 treatment at 11 nmol/kg/d (PN/GLP-2, n = 7). At terminal laparotomy, bile and liver samples were collected. The relative gene expression of enzymes involved in bile acid synthesis, regulation, and transport was measured in liver by reverse-transcriptase quantitative polymerase chain reaction. Bile acid composition in bile was determined using tandem mass spectrometry. Data were analyzed using 1-way analysis of variance (ANOVA) or Kruskal-Wallis ANOVA. Results: GLP-2 increased the expression of bile acid export genes: multidrug resistance-associated proteins 2 (MRP2) (P = .002) and 3 (MRP3) (P = .037) over saline control. GLP-2 increased expression of Farnesoid X receptor (FXR) (P < .001) and CYP7A1 (cytochrome P450, family 7, subfamily A, polypeptide 1) (P = .03). GLP-2 treatment was associated with decreased concentrations of Taurohyocholic Acid and conjugates of toxic lithocholic acid (P < .01). GLP-2 treatment increased the liver bile acid content. Conclusions: GLP-2 treatment was associated with alterations in the hepatic expression of genes involved in bile acid metabolism. The transcriptomic results indicate the mechanisms at the transcriptional level acting to regulate bile acid synthesis and increase bile acid export. Differences in bile acid profiles further support a beneficial role for GLP-2 therapy in PNALD.
Dietary Macroalgae Saccharina japonica Ameliorates Liver Injury Induced by a High-Carbohydrate Diet in Swamp Eel ( Monopterus albus)
Front Vet Sci 2022 Jun 14;9:869369.PMID:35774985DOI:10.3389/fvets.2022.869369.
A high-carbohydrate diet lowers the rearing cost and decreases the ammonia emission into the environment, whereas it can induce liver injury, which can reduce harvest yields and generate economic losses in reared fish species. Macroalgae Saccharina japonica (SJ) has been reported to improve anti-diabetic, but the protective mechanism of dietary SJ against liver injury in fish fed a high-carbohydrate diet has not been studied. Therefore, a 56-day nutritional trial was designed for swamp eel Monopterus albus, which was fed with the normal diet [20% carbohydrate, normal carbohydrate (NC)], a high carbohydrate diet (32% carbohydrate, HC), and a HC diet supplemented with 2.5% SJ (HC-S). The HC diet promoted growth and lowered feed coefficient (FC), whereas it increased hepatosomatic index (HSI) when compared with the NC diet in this study. However, SJ supplementation increased iodine contents in muscle, reduced HSI, and improved liver injury, such as the decrease of glucose (GLU), total bile acid (TBA), and alanine aminotransferase (ALT) in serum, and glycogen and TBA in the liver. Consistently, histological analysis showed that SJ reduced the area of lipid droplet, glycogen, and collagen fiber in the liver (p < 0.05). Thoroughly, the underlying protective mechanisms of SJ supplementation against HC-induced liver injury were studied by liver transcriptome sequencing coupled with pathway analysis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the differentially expressed genes (DEGs), such as the acetyl-coenzyme A synthetase (acss1), alcohol dehydrogenase (adh), interferon-induced protein with tetratricopeptide repeats 1 (ifit1), aldo-keto reductase family 1 member D1 (akr1d1), cholesterol 7-alpha-monooxygenase (cyp7a1), and UDP-glucuronosyltransferase (ugt), indicated that the pathway of glycolysis/gluconeogenesis was the main metabolic pathway altered in the HC group compared with the NC group. Meanwhile, hepatitis C, primary BA biosynthesis, and drug metabolism-cytochrome P450 were the three main metabolic pathways altered by SJ supplementation when compared with the HC group. Moreover, the BA-targeted metabolomic analysis of the serum BA found that SJ supplementation decreased the contents of Taurohyocholic Acid (THCA), taurochenodeoxycholic acid (TCDCA), taurolithocholic acid (TLCA), nordeoxycholic acid (NorDCA), and increased the contents of ursocholic acid (UCA), allocholic acid (ACA), and chenodeoxycholic acid (CDCA). In particular, the higher contents of UCA, ACA, and CDCA regulated by SJ were associated with lower liver injury. Overall, these results indicate that the 2.5% supplementation of SJ can be recommended as a functional feed additive for the alleviation of liver injury in swamp eel-fed high-carbohydrate diets.
Targeted metabolomics study of serum bile acid profile in patients with end-stage renal disease undergoing hemodialysis
PeerJ 2019 Jun 17;7:e7145.PMID:31245185DOI:10.7717/peerj.7145.
Background: Bile acids are important metabolites of intestinal microbiota, which have profound effects on host health. However, whether metabolism of bile acids is involved in the metabolic complications of end-stage renal disease (ESRD), and the effects of bile acids on the prognosis of ESRD remain obscure. Therefore, this study investigated the relationship between altered bile acid profile and the prognosis of ESRD patients. Methods: A targeted metabolomics approach based on ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was used to determine the changes in serum bile acids between ESRD patients (n = 77) and healthy controls (n = 30). Univariate and multivariate statistical analyses were performed to screen the differential proportions of bile acids between the two groups. Results: Six differentially expressed bile acids were identified as potential biomarkers for differentiating ESRD patients from healthy subjects. The decreased concentrations of chenodeoxycholic acid, deoxycholic acid and cholic acid were significantly associated with dyslipidemia in ESRD patients. Subgroup analyses revealed that the significantly increased concentrations of taurocholic acid, taurochenodeoxycholic acid, Taurohyocholic Acid and tauro α-muricholic acid were correlated to the poor prognosis of ESRD patients. Conclusions: The serum bile acid profile of ESRD patients differed significantly from that of healthy controls. In addition, the altered serum bile acid profile might contribute to the poor prognosis and metabolic complications of ESRD patients.
Effect of Weaning at 21 Days of Age on the Content of Bile Acids in Chyme of Cecum
Animals (Basel) 2022 Aug 20;12(16):2138.PMID:36009728DOI:10.3390/ani12162138.
This experiment was conducted to investigate the effects of weaning at 21 days of age on cecal chyme bile acids (BAs) in piglets. According to a 2 × 3 factorial design, the main factors were lactation and weaning, and the other factor was 22, 24, and 28 days of age, respectively. Piglets were randomly divided into two groups of eighteen piglets each and six piglets were selected for slaughter at 22, 24, and 28 days of age, respectively, to determine the content of different types of Bas in the intestinal lumen of the cecum. Results: (1) There was a significant interaction between weaning and age on intestinal primary Bas hyocholic acid (HCA) and chenodeoxycholic acid (CDCA) (p < 0.05), and weaning significantly increased the content of primary BAs in piglets’ intestines, which showed a trend of decreasing and then increasing with the increase in piglets’ age. (2) There was a significant interaction between weaning and age on intestinal secondary BAs deoxycholic acid (DCA), lithocholic acid (LCA), and ursodeoxycholic acid (UDCA) (p < 0.05). DCA and LCA in piglets’ intestines tended to decrease with increasing age, while UDCA showed a trend of decreasing and then increasing with increasing piglets’ age; weaning significantly increased the content of secondary BAs in piglets’ intestines. (3) There was a significant interaction between weaning and age on intestinal glycine chenodeoxycholic acid (GCDCA), taurochenodeoxycholic acid (TCDCA), and taurolithocholic acid (TLCA), but not on Taurohyocholic Acid (THCA), taurohyodeoxycholic acid (THDCA), and taurineursodeoxycholic acid (TUDCA) (p > 0.05). Weaning significantly increased the contents of GCDCA, TCDCA, TLCA, THDCA, and TUDCA in the intestinal tract (p < 0.05), while THCA content was not significant. In conclusion, weaning can increase the BAs content in the cecum of piglets, and there is an interaction between group and weaning age on BAs content.