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Ambeed Inc sodium salt tdca
: Metallobsh gene abundance inversely correlates with taurine-conjugated BA levels in the small intestine and stool. The log 2 (read count) of metalloBSH-encoding genes in metagenomes from the pyloric sphincter (Capsule 1), small intestine (Capsule 2 and 3), and stool negatively correlated with nearly all detected taurine-conjugated BAs in paired metabolomes. These inverse correlations are highly significant for TCA (9a), TCDCA (9b), <t>TUDCA</t> (9c), and T-⍺-MCA (9d), with weaker or non-significant correlations observed for <t>TDCA</t> (9e, Capsule 2 P adj = 0.085) and TLCA (9f, Capsule 2, P adj = 0.055). Conversely, no significant correlations between metalloBSH abundance and taurine-conjugated BA levels were observed in the ascending colon (Capsule 4). Statistics reflect Spearman correlations with Benjamini–Hochberg correction. Data points represent individual samples with paired metagenomic and metabolomic data (Capsule 1, N = 51; Capsule 2, N= 59; Capsule 3, N = 55; Capsule 4, N = 44; Stool, N =56).
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1) Product Images from "A previously unappreciated class of metal-dependent bile salt hydrolases from the human gut microbiome"

Article Title: A previously unappreciated class of metal-dependent bile salt hydrolases from the human gut microbiome

Journal: bioRxiv

doi: 10.64898/2026.04.05.716592

: Metallobsh gene abundance inversely correlates with taurine-conjugated BA levels in the small intestine and stool. The log 2 (read count) of metalloBSH-encoding genes in metagenomes from the pyloric sphincter (Capsule 1), small intestine (Capsule 2 and 3), and stool negatively correlated with nearly all detected taurine-conjugated BAs in paired metabolomes. These inverse correlations are highly significant for TCA (9a), TCDCA (9b), TUDCA (9c), and T-⍺-MCA (9d), with weaker or non-significant correlations observed for TDCA (9e, Capsule 2 P adj = 0.085) and TLCA (9f, Capsule 2, P adj = 0.055). Conversely, no significant correlations between metalloBSH abundance and taurine-conjugated BA levels were observed in the ascending colon (Capsule 4). Statistics reflect Spearman correlations with Benjamini–Hochberg correction. Data points represent individual samples with paired metagenomic and metabolomic data (Capsule 1, N = 51; Capsule 2, N= 59; Capsule 3, N = 55; Capsule 4, N = 44; Stool, N =56).
Figure Legend Snippet: : Metallobsh gene abundance inversely correlates with taurine-conjugated BA levels in the small intestine and stool. The log 2 (read count) of metalloBSH-encoding genes in metagenomes from the pyloric sphincter (Capsule 1), small intestine (Capsule 2 and 3), and stool negatively correlated with nearly all detected taurine-conjugated BAs in paired metabolomes. These inverse correlations are highly significant for TCA (9a), TCDCA (9b), TUDCA (9c), and T-⍺-MCA (9d), with weaker or non-significant correlations observed for TDCA (9e, Capsule 2 P adj = 0.085) and TLCA (9f, Capsule 2, P adj = 0.055). Conversely, no significant correlations between metalloBSH abundance and taurine-conjugated BA levels were observed in the ascending colon (Capsule 4). Statistics reflect Spearman correlations with Benjamini–Hochberg correction. Data points represent individual samples with paired metagenomic and metabolomic data (Capsule 1, N = 51; Capsule 2, N= 59; Capsule 3, N = 55; Capsule 4, N = 44; Stool, N =56).

Techniques Used: Metabolomic



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Ambeed Inc sodium salt tdca
: Metallobsh gene abundance inversely correlates with taurine-conjugated BA levels in the small intestine and stool. The log 2 (read count) of metalloBSH-encoding genes in metagenomes from the pyloric sphincter (Capsule 1), small intestine (Capsule 2 and 3), and stool negatively correlated with nearly all detected taurine-conjugated BAs in paired metabolomes. These inverse correlations are highly significant for TCA (9a), TCDCA (9b), <t>TUDCA</t> (9c), and T-⍺-MCA (9d), with weaker or non-significant correlations observed for <t>TDCA</t> (9e, Capsule 2 P adj = 0.085) and TLCA (9f, Capsule 2, P adj = 0.055). Conversely, no significant correlations between metalloBSH abundance and taurine-conjugated BA levels were observed in the ascending colon (Capsule 4). Statistics reflect Spearman correlations with Benjamini–Hochberg correction. Data points represent individual samples with paired metagenomic and metabolomic data (Capsule 1, N = 51; Capsule 2, N= 59; Capsule 3, N = 55; Capsule 4, N = 44; Stool, N =56).
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: Metallobsh gene abundance inversely correlates with taurine-conjugated BA levels in the small intestine and stool. The log 2 (read count) of metalloBSH-encoding genes in metagenomes from the pyloric sphincter (Capsule 1), small intestine (Capsule 2 and 3), and stool negatively correlated with nearly all detected taurine-conjugated BAs in paired metabolomes. These inverse correlations are highly significant for TCA (9a), TCDCA (9b), <t>TUDCA</t> (9c), and T-⍺-MCA (9d), with weaker or non-significant correlations observed for <t>TDCA</t> (9e, Capsule 2 P adj = 0.085) and TLCA (9f, Capsule 2, P adj = 0.055). Conversely, no significant correlations between metalloBSH abundance and taurine-conjugated BA levels were observed in the ascending colon (Capsule 4). Statistics reflect Spearman correlations with Benjamini–Hochberg correction. Data points represent individual samples with paired metagenomic and metabolomic data (Capsule 1, N = 51; Capsule 2, N= 59; Capsule 3, N = 55; Capsule 4, N = 44; Stool, N =56).
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MRM chromatograms of all quantitative BAs. 1. TωMCA, 2. TαMCA, 3. TβMCA, 4. THCA, 5. <t>TUDCA,</t> 6. THDCA, 7. TCA, 8. ωMCA, 9. αMCA, 10. GCA, 11. βMCA, 12. TCDCA, 13. <t>TDCA,</t> 14. CA, 15. UDCA, 16. HDCA, 17. GCDCA, and 18. CDCA.
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MRM chromatograms of all quantitative BAs. 1. TωMCA, 2. TαMCA, 3. TβMCA, 4. THCA, 5. <t>TUDCA,</t> 6. THDCA, 7. TCA, 8. ωMCA, 9. αMCA, 10. GCA, 11. βMCA, 12. TCDCA, 13. <t>TDCA,</t> 14. CA, 15. UDCA, 16. HDCA, 17. GCDCA, and 18. CDCA.
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MRM chromatograms of all quantitative BAs. 1. TωMCA, 2. TαMCA, 3. TβMCA, 4. THCA, 5. <t>TUDCA,</t> 6. THDCA, 7. TCA, 8. ωMCA, 9. αMCA, 10. GCA, 11. βMCA, 12. TCDCA, 13. <t>TDCA,</t> 14. CA, 15. UDCA, 16. HDCA, 17. GCDCA, and 18. CDCA.
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Fig. 4. A simplified diagram of bile acid biosynthesis, the alteration of serum cholesterol, bile acid, conjugated bile acids and their total levels in each animal group. Data expressed as mean ± SEM. One-way ANOVA, LSD post-Hoc test compared with HFD-fed model. *p < 0.05, **p < 0.01, ***p < 0.001. Control, normal control group; HFD, HFD group; PCRR-H, PCRR-H treated group (n = 6–7). Orange boxes with ↑ mean increased serum level; a blue box with ↓ means a decreased serum level in the PCRR-H-treated group compared with the HFD group; white boxes mean no significant change. α-MCA, α-Muricholate; β-MCA, β-muricholate; CA, cholate; CDCA, chenodeoxycholate; DCA, deoxycholate; GCA, glycocholate; GCDCA, glycochenodeoxycholate; GDCA, glycodeoxycholate; GHDCA, glyco chenodeoxycholate; GUDCA, glycoursodeoxycholate; HDCA, hyodeoxycholate; LCA, lithocholate; TCA, taurocholate; TCDCA, taurochenodeoxycholate; <t>TDCA,</t> ursodeoxycholate; THDCA, taurohyodeoxycholate; <t>TUDCA,</t> <t>tauroursodeoxycholate;</t> UDCA, ursodeoxycholate; N.S., not significant; N.D., not detected. Dotted line: skipped pathway.
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Fig. 4. A simplified diagram of bile acid biosynthesis, the alteration of serum cholesterol, bile acid, conjugated bile acids and their total levels in each animal group. Data expressed as mean ± SEM. One-way ANOVA, LSD post-Hoc test compared with HFD-fed model. *p < 0.05, **p < 0.01, ***p < 0.001. Control, normal control group; HFD, HFD group; PCRR-H, PCRR-H treated group (n = 6–7). Orange boxes with ↑ mean increased serum level; a blue box with ↓ means a decreased serum level in the PCRR-H-treated group compared with the HFD group; white boxes mean no significant change. α-MCA, α-Muricholate; β-MCA, β-muricholate; CA, cholate; CDCA, chenodeoxycholate; DCA, deoxycholate; GCA, glycocholate; GCDCA, glycochenodeoxycholate; GDCA, glycodeoxycholate; GHDCA, glyco chenodeoxycholate; GUDCA, glycoursodeoxycholate; HDCA, hyodeoxycholate; LCA, lithocholate; TCA, taurocholate; TCDCA, taurochenodeoxycholate; <t>TDCA,</t> ursodeoxycholate; THDCA, taurohyodeoxycholate; <t>TUDCA,</t> <t>tauroursodeoxycholate;</t> UDCA, ursodeoxycholate; N.S., not significant; N.D., not detected. Dotted line: skipped pathway.
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Fig. 4. A simplified diagram of bile acid biosynthesis, the alteration of serum cholesterol, bile acid, conjugated bile acids and their total levels in each animal group. Data expressed as mean ± SEM. One-way ANOVA, LSD post-Hoc test compared with HFD-fed model. *p < 0.05, **p < 0.01, ***p < 0.001. Control, normal control group; HFD, HFD group; PCRR-H, PCRR-H treated group (n = 6–7). Orange boxes with ↑ mean increased serum level; a blue box with ↓ means a decreased serum level in the PCRR-H-treated group compared with the HFD group; white boxes mean no significant change. α-MCA, α-Muricholate; β-MCA, β-muricholate; CA, cholate; CDCA, chenodeoxycholate; DCA, deoxycholate; GCA, glycocholate; GCDCA, glycochenodeoxycholate; GDCA, glycodeoxycholate; GHDCA, glyco chenodeoxycholate; GUDCA, glycoursodeoxycholate; HDCA, hyodeoxycholate; LCA, lithocholate; TCA, taurocholate; TCDCA, taurochenodeoxycholate; <t>TDCA,</t> ursodeoxycholate; THDCA, taurohyodeoxycholate; <t>TUDCA,</t> <t>tauroursodeoxycholate;</t> UDCA, ursodeoxycholate; N.S., not significant; N.D., not detected. Dotted line: skipped pathway.
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: Metallobsh gene abundance inversely correlates with taurine-conjugated BA levels in the small intestine and stool. The log 2 (read count) of metalloBSH-encoding genes in metagenomes from the pyloric sphincter (Capsule 1), small intestine (Capsule 2 and 3), and stool negatively correlated with nearly all detected taurine-conjugated BAs in paired metabolomes. These inverse correlations are highly significant for TCA (9a), TCDCA (9b), TUDCA (9c), and T-⍺-MCA (9d), with weaker or non-significant correlations observed for TDCA (9e, Capsule 2 P adj = 0.085) and TLCA (9f, Capsule 2, P adj = 0.055). Conversely, no significant correlations between metalloBSH abundance and taurine-conjugated BA levels were observed in the ascending colon (Capsule 4). Statistics reflect Spearman correlations with Benjamini–Hochberg correction. Data points represent individual samples with paired metagenomic and metabolomic data (Capsule 1, N = 51; Capsule 2, N= 59; Capsule 3, N = 55; Capsule 4, N = 44; Stool, N =56).

Journal: bioRxiv

Article Title: A previously unappreciated class of metal-dependent bile salt hydrolases from the human gut microbiome

doi: 10.64898/2026.04.05.716592

Figure Lengend Snippet: : Metallobsh gene abundance inversely correlates with taurine-conjugated BA levels in the small intestine and stool. The log 2 (read count) of metalloBSH-encoding genes in metagenomes from the pyloric sphincter (Capsule 1), small intestine (Capsule 2 and 3), and stool negatively correlated with nearly all detected taurine-conjugated BAs in paired metabolomes. These inverse correlations are highly significant for TCA (9a), TCDCA (9b), TUDCA (9c), and T-⍺-MCA (9d), with weaker or non-significant correlations observed for TDCA (9e, Capsule 2 P adj = 0.085) and TLCA (9f, Capsule 2, P adj = 0.055). Conversely, no significant correlations between metalloBSH abundance and taurine-conjugated BA levels were observed in the ascending colon (Capsule 4). Statistics reflect Spearman correlations with Benjamini–Hochberg correction. Data points represent individual samples with paired metagenomic and metabolomic data (Capsule 1, N = 51; Capsule 2, N= 59; Capsule 3, N = 55; Capsule 4, N = 44; Stool, N =56).

Article Snippet: Taurodeoxycholic acid, sodium salt (TDCA) was purchased from AmBeed.

Techniques: Metabolomic

MRM chromatograms of all quantitative BAs. 1. TωMCA, 2. TαMCA, 3. TβMCA, 4. THCA, 5. TUDCA, 6. THDCA, 7. TCA, 8. ωMCA, 9. αMCA, 10. GCA, 11. βMCA, 12. TCDCA, 13. TDCA, 14. CA, 15. UDCA, 16. HDCA, 17. GCDCA, and 18. CDCA.

Journal: Frontiers in Physiology

Article Title: Profiling bile acid composition in bile from mice of different ages and sexes

doi: 10.3389/fphys.2025.1626215

Figure Lengend Snippet: MRM chromatograms of all quantitative BAs. 1. TωMCA, 2. TαMCA, 3. TβMCA, 4. THCA, 5. TUDCA, 6. THDCA, 7. TCA, 8. ωMCA, 9. αMCA, 10. GCA, 11. βMCA, 12. TCDCA, 13. TDCA, 14. CA, 15. UDCA, 16. HDCA, 17. GCDCA, and 18. CDCA.

Article Snippet: BA standards, including cholic acid (CA) (Cat. No. C1900-015), glycocholic acid (GCA) (Cat. No. C1925-000), taurocholic acid (TCA) (Cat. No. C1965-000), CDCA (Cat. No. C0940-000), glycochenodeoxycholic acid (GCDCA) (Cat. No. C0962-000), taurochenodeoxycholic acid (TCDCA) (Cat. No. C0990-000), α-muricholic acid (αMCA) (Cat. No. C1890-000), β-muricholic acid (βMCA) (Cat. No. C1895-000), tauro α-muricholic acid (TαMCA) (Cat. No. C1893-000), tauro β-muricholic acid (TβMCA) (Cat. No. C1899-000), ursodeoxycholic acid (UDCA) (Cat. No. C1020-000), TUDCA (Cat. No. C1052-000), taurodeoxycholic acid (TDCA) (Cat. No. C1162-000), taurohyocholic acid (THCA) (Cat. No. C1887-000), HDCA (Cat. No. C0860-000), taurohyodeoxycholic acid (THDCA) (Cat. No. C0892-000), ω-muricholic acid (ωMCA) (Cat. No. C1888-000), and tauro ω-muricholic acid (TωMCA) (Cat. No. C1889-000) were purchased from Steraloids Inc. (Newport, RI, United States).

Techniques:

Comparison of TBA levels and BA composition in 8-week-old and 60-week-old mice. (A) TBA levels at the two ages. (B) PCBA, PUBA, SCBA, and SUBA levels at the two ages. (C) BA percentage compositions at the two ages. (D) Individual BA levels at the two ages. TBAs, total BAs, the sum of all individual BAs detected; 8W, 8-week; 60W, 60-week; PCBAs: TCA, GCA, TCDCA, GCDCA, TαMCA, TβMCA, and TUDCA; PUBAs: CA, CDCA, αMCA, βMCA, and UDCA; SCBAs: TωMCA, TDCA, THCA, and THDCA; SUBAs: ωMCA and HDCA; *p < 0.05 and **p < 0.01; sample size: n = 24 for 8W and n = 28 for 60W.

Journal: Frontiers in Physiology

Article Title: Profiling bile acid composition in bile from mice of different ages and sexes

doi: 10.3389/fphys.2025.1626215

Figure Lengend Snippet: Comparison of TBA levels and BA composition in 8-week-old and 60-week-old mice. (A) TBA levels at the two ages. (B) PCBA, PUBA, SCBA, and SUBA levels at the two ages. (C) BA percentage compositions at the two ages. (D) Individual BA levels at the two ages. TBAs, total BAs, the sum of all individual BAs detected; 8W, 8-week; 60W, 60-week; PCBAs: TCA, GCA, TCDCA, GCDCA, TαMCA, TβMCA, and TUDCA; PUBAs: CA, CDCA, αMCA, βMCA, and UDCA; SCBAs: TωMCA, TDCA, THCA, and THDCA; SUBAs: ωMCA and HDCA; *p < 0.05 and **p < 0.01; sample size: n = 24 for 8W and n = 28 for 60W.

Article Snippet: BA standards, including cholic acid (CA) (Cat. No. C1900-015), glycocholic acid (GCA) (Cat. No. C1925-000), taurocholic acid (TCA) (Cat. No. C1965-000), CDCA (Cat. No. C0940-000), glycochenodeoxycholic acid (GCDCA) (Cat. No. C0962-000), taurochenodeoxycholic acid (TCDCA) (Cat. No. C0990-000), α-muricholic acid (αMCA) (Cat. No. C1890-000), β-muricholic acid (βMCA) (Cat. No. C1895-000), tauro α-muricholic acid (TαMCA) (Cat. No. C1893-000), tauro β-muricholic acid (TβMCA) (Cat. No. C1899-000), ursodeoxycholic acid (UDCA) (Cat. No. C1020-000), TUDCA (Cat. No. C1052-000), taurodeoxycholic acid (TDCA) (Cat. No. C1162-000), taurohyocholic acid (THCA) (Cat. No. C1887-000), HDCA (Cat. No. C0860-000), taurohyodeoxycholic acid (THDCA) (Cat. No. C0892-000), ω-muricholic acid (ωMCA) (Cat. No. C1888-000), and tauro ω-muricholic acid (TωMCA) (Cat. No. C1889-000) were purchased from Steraloids Inc. (Newport, RI, United States).

Techniques: Comparison

Fig. 4. A simplified diagram of bile acid biosynthesis, the alteration of serum cholesterol, bile acid, conjugated bile acids and their total levels in each animal group. Data expressed as mean ± SEM. One-way ANOVA, LSD post-Hoc test compared with HFD-fed model. *p < 0.05, **p < 0.01, ***p < 0.001. Control, normal control group; HFD, HFD group; PCRR-H, PCRR-H treated group (n = 6–7). Orange boxes with ↑ mean increased serum level; a blue box with ↓ means a decreased serum level in the PCRR-H-treated group compared with the HFD group; white boxes mean no significant change. α-MCA, α-Muricholate; β-MCA, β-muricholate; CA, cholate; CDCA, chenodeoxycholate; DCA, deoxycholate; GCA, glycocholate; GCDCA, glycochenodeoxycholate; GDCA, glycodeoxycholate; GHDCA, glyco chenodeoxycholate; GUDCA, glycoursodeoxycholate; HDCA, hyodeoxycholate; LCA, lithocholate; TCA, taurocholate; TCDCA, taurochenodeoxycholate; TDCA, ursodeoxycholate; THDCA, taurohyodeoxycholate; TUDCA, tauroursodeoxycholate; UDCA, ursodeoxycholate; N.S., not significant; N.D., not detected. Dotted line: skipped pathway.

Journal: Pharmacological Research - Modern Chinese Medicine

Article Title: Polygoni Cuspidati Rhizoma et Radix extract attenuates high-fat diet-induced NAFLD in rats: impact on untargeted serum metabolomics and liver lipidomics

doi: 10.1016/j.prmcm.2023.100335

Figure Lengend Snippet: Fig. 4. A simplified diagram of bile acid biosynthesis, the alteration of serum cholesterol, bile acid, conjugated bile acids and their total levels in each animal group. Data expressed as mean ± SEM. One-way ANOVA, LSD post-Hoc test compared with HFD-fed model. *p < 0.05, **p < 0.01, ***p < 0.001. Control, normal control group; HFD, HFD group; PCRR-H, PCRR-H treated group (n = 6–7). Orange boxes with ↑ mean increased serum level; a blue box with ↓ means a decreased serum level in the PCRR-H-treated group compared with the HFD group; white boxes mean no significant change. α-MCA, α-Muricholate; β-MCA, β-muricholate; CA, cholate; CDCA, chenodeoxycholate; DCA, deoxycholate; GCA, glycocholate; GCDCA, glycochenodeoxycholate; GDCA, glycodeoxycholate; GHDCA, glyco chenodeoxycholate; GUDCA, glycoursodeoxycholate; HDCA, hyodeoxycholate; LCA, lithocholate; TCA, taurocholate; TCDCA, taurochenodeoxycholate; TDCA, ursodeoxycholate; THDCA, taurohyodeoxycholate; TUDCA, tauroursodeoxycholate; UDCA, ursodeoxycholate; N.S., not significant; N.D., not detected. Dotted line: skipped pathway.

Article Snippet: Other internal standards [D-glucose (U-13C6), cholic acid-2,2,4,4-D4 and L-tryptophan(indole-D5)], and glycoursodeoxycholic acid (GUDCA) were acquired from Cambridge Isotope Laboratories (Tewksbury, MA, USA). α-Muricholic acid (α-MA), deoxycholic acid (DCA), and taurodeoxycholic acid (TDCA) were purchased from Santa Cruz Biotechnology (Dallas, Texas, USA).

Techniques: Control