Cysteine sulfinic acid decarboxylase regulation

A role for farnesoid X receptor and small heterodimer partner in murine hepatic taurine metabolism

Thomas A. Kerr, Yuri Matsumoto, Hitoshi Matsumoto, Yan Xie, Lawrence L. Hirschberger, Martha H. Stipanuk, Sayeepriyadarshini Anakk, David D. Moore, Mitsuhiro Watanabe, Susan Kennedy, Nicholas O. Davidson

Research output: Contribution to journalArticle

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Abstract

Aim: Bile acid synthesis is regulated by nuclear receptors including farnesoid X receptor (FXR) and small heterodimer partner (SHP), and by fibroblast growth factor 15/19 (FGF15/19). We hypothesized that hepatic cysteine sulfinic acid decarboxylase (CSAD) (a key enzyme in taurine synthesis) is regulated by bile acids (BA). The aim of this study was to investigate CSAD regulation by BA dependent regulatory mechanisms. Methods: Mice were fed a control diet or a diet supplemented with either 0.5% cholate or 2% cholestyramine. To study BA dependent pathways, we utilized GW4064 (FXR agonist), FGF19 or T-0901317 (liver X receptor [LXR] agonist) and Shp-/- mice. Tissue mRNA was determined by quantitative reverse transcription polymerase chain reaction. Amino acids were measured by high-performance liquid chromatography. Results: Mice supplemented with dietary cholate exhibited reduced hepatic CSAD mRNA while those receiving cholestyramine exhibited increased mRNA. Activation of FXR suppressed CSAD mRNA expression whereas CSAD expression was increased in Shp-/- mice. Hepatic hypotaurine concentration (the product of CSAD) was higher in Shp-/- mice with a corresponding increase in serum taurine conjugated BA. FGF19 administration suppressed hepatic cholesterol 7-α-hydroxylase (CYP7A1) mRNA but did not change CSAD mRNA expression. LXR activation induced CYP7A1 mRNA yet failed to induce CSAD mRNA expression. Conclusion: BA regulate CSAD mRNA expression in a feedback fashion via mechanisms involving SHP and FXR but not FGF15/19 or LXR. These findings implicate BA as regulators of CSAD mRNA via mechanisms shared with CYP7A1.

Original languageEnglish
Pages (from-to)E218-E228
JournalHepatology Research
Volume44
Issue number10
DOIs
Publication statusPublished - 2014 Oct 1

Fingerprint

sulfoalanine decarboxylase
Taurine
Bile Acids and Salts
Messenger RNA
Liver
Cholates
Cholestyramine Resin
Cholesterol 7-alpha-Hydroxylase
Diet
Fibroblast Growth Factor Receptors
Fibroblast Growth Factors
Cytoplasmic and Nuclear Receptors

Keywords

  • Bile acid conjugation
  • Bile acid metabolism
  • Nuclear hormone receptors
  • Taurine synthesis

ASJC Scopus subject areas

  • Hepatology
  • Infectious Diseases

Cite this

Kerr, T. A., Matsumoto, Y., Matsumoto, H., Xie, Y., Hirschberger, L. L., Stipanuk, M. H., ... Davidson, N. O. (2014). Cysteine sulfinic acid decarboxylase regulation: A role for farnesoid X receptor and small heterodimer partner in murine hepatic taurine metabolism. Hepatology Research, 44(10), E218-E228. https://doi.org/10.1111/hepr.12230

Cysteine sulfinic acid decarboxylase regulation : A role for farnesoid X receptor and small heterodimer partner in murine hepatic taurine metabolism. / Kerr, Thomas A.; Matsumoto, Yuri; Matsumoto, Hitoshi; Xie, Yan; Hirschberger, Lawrence L.; Stipanuk, Martha H.; Anakk, Sayeepriyadarshini; Moore, David D.; Watanabe, Mitsuhiro; Kennedy, Susan; Davidson, Nicholas O.

In: Hepatology Research, Vol. 44, No. 10, 01.10.2014, p. E218-E228.

Research output: Contribution to journalArticle

Kerr, TA, Matsumoto, Y, Matsumoto, H, Xie, Y, Hirschberger, LL, Stipanuk, MH, Anakk, S, Moore, DD, Watanabe, M, Kennedy, S & Davidson, NO 2014, 'Cysteine sulfinic acid decarboxylase regulation: A role for farnesoid X receptor and small heterodimer partner in murine hepatic taurine metabolism', Hepatology Research, vol. 44, no. 10, pp. E218-E228. https://doi.org/10.1111/hepr.12230
Kerr, Thomas A. ; Matsumoto, Yuri ; Matsumoto, Hitoshi ; Xie, Yan ; Hirschberger, Lawrence L. ; Stipanuk, Martha H. ; Anakk, Sayeepriyadarshini ; Moore, David D. ; Watanabe, Mitsuhiro ; Kennedy, Susan ; Davidson, Nicholas O. / Cysteine sulfinic acid decarboxylase regulation : A role for farnesoid X receptor and small heterodimer partner in murine hepatic taurine metabolism. In: Hepatology Research. 2014 ; Vol. 44, No. 10. pp. E218-E228.
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abstract = "Aim: Bile acid synthesis is regulated by nuclear receptors including farnesoid X receptor (FXR) and small heterodimer partner (SHP), and by fibroblast growth factor 15/19 (FGF15/19). We hypothesized that hepatic cysteine sulfinic acid decarboxylase (CSAD) (a key enzyme in taurine synthesis) is regulated by bile acids (BA). The aim of this study was to investigate CSAD regulation by BA dependent regulatory mechanisms. Methods: Mice were fed a control diet or a diet supplemented with either 0.5{\%} cholate or 2{\%} cholestyramine. To study BA dependent pathways, we utilized GW4064 (FXR agonist), FGF19 or T-0901317 (liver X receptor [LXR] agonist) and Shp-/- mice. Tissue mRNA was determined by quantitative reverse transcription polymerase chain reaction. Amino acids were measured by high-performance liquid chromatography. Results: Mice supplemented with dietary cholate exhibited reduced hepatic CSAD mRNA while those receiving cholestyramine exhibited increased mRNA. Activation of FXR suppressed CSAD mRNA expression whereas CSAD expression was increased in Shp-/- mice. Hepatic hypotaurine concentration (the product of CSAD) was higher in Shp-/- mice with a corresponding increase in serum taurine conjugated BA. FGF19 administration suppressed hepatic cholesterol 7-α-hydroxylase (CYP7A1) mRNA but did not change CSAD mRNA expression. LXR activation induced CYP7A1 mRNA yet failed to induce CSAD mRNA expression. Conclusion: BA regulate CSAD mRNA expression in a feedback fashion via mechanisms involving SHP and FXR but not FGF15/19 or LXR. These findings implicate BA as regulators of CSAD mRNA via mechanisms shared with CYP7A1.",
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T2 - A role for farnesoid X receptor and small heterodimer partner in murine hepatic taurine metabolism

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AU - Matsumoto, Yuri

AU - Matsumoto, Hitoshi

AU - Xie, Yan

AU - Hirschberger, Lawrence L.

AU - Stipanuk, Martha H.

AU - Anakk, Sayeepriyadarshini

AU - Moore, David D.

AU - Watanabe, Mitsuhiro

AU - Kennedy, Susan

AU - Davidson, Nicholas O.

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N2 - Aim: Bile acid synthesis is regulated by nuclear receptors including farnesoid X receptor (FXR) and small heterodimer partner (SHP), and by fibroblast growth factor 15/19 (FGF15/19). We hypothesized that hepatic cysteine sulfinic acid decarboxylase (CSAD) (a key enzyme in taurine synthesis) is regulated by bile acids (BA). The aim of this study was to investigate CSAD regulation by BA dependent regulatory mechanisms. Methods: Mice were fed a control diet or a diet supplemented with either 0.5% cholate or 2% cholestyramine. To study BA dependent pathways, we utilized GW4064 (FXR agonist), FGF19 or T-0901317 (liver X receptor [LXR] agonist) and Shp-/- mice. Tissue mRNA was determined by quantitative reverse transcription polymerase chain reaction. Amino acids were measured by high-performance liquid chromatography. Results: Mice supplemented with dietary cholate exhibited reduced hepatic CSAD mRNA while those receiving cholestyramine exhibited increased mRNA. Activation of FXR suppressed CSAD mRNA expression whereas CSAD expression was increased in Shp-/- mice. Hepatic hypotaurine concentration (the product of CSAD) was higher in Shp-/- mice with a corresponding increase in serum taurine conjugated BA. FGF19 administration suppressed hepatic cholesterol 7-α-hydroxylase (CYP7A1) mRNA but did not change CSAD mRNA expression. LXR activation induced CYP7A1 mRNA yet failed to induce CSAD mRNA expression. Conclusion: BA regulate CSAD mRNA expression in a feedback fashion via mechanisms involving SHP and FXR but not FGF15/19 or LXR. These findings implicate BA as regulators of CSAD mRNA via mechanisms shared with CYP7A1.

AB - Aim: Bile acid synthesis is regulated by nuclear receptors including farnesoid X receptor (FXR) and small heterodimer partner (SHP), and by fibroblast growth factor 15/19 (FGF15/19). We hypothesized that hepatic cysteine sulfinic acid decarboxylase (CSAD) (a key enzyme in taurine synthesis) is regulated by bile acids (BA). The aim of this study was to investigate CSAD regulation by BA dependent regulatory mechanisms. Methods: Mice were fed a control diet or a diet supplemented with either 0.5% cholate or 2% cholestyramine. To study BA dependent pathways, we utilized GW4064 (FXR agonist), FGF19 or T-0901317 (liver X receptor [LXR] agonist) and Shp-/- mice. Tissue mRNA was determined by quantitative reverse transcription polymerase chain reaction. Amino acids were measured by high-performance liquid chromatography. Results: Mice supplemented with dietary cholate exhibited reduced hepatic CSAD mRNA while those receiving cholestyramine exhibited increased mRNA. Activation of FXR suppressed CSAD mRNA expression whereas CSAD expression was increased in Shp-/- mice. Hepatic hypotaurine concentration (the product of CSAD) was higher in Shp-/- mice with a corresponding increase in serum taurine conjugated BA. FGF19 administration suppressed hepatic cholesterol 7-α-hydroxylase (CYP7A1) mRNA but did not change CSAD mRNA expression. LXR activation induced CYP7A1 mRNA yet failed to induce CSAD mRNA expression. Conclusion: BA regulate CSAD mRNA expression in a feedback fashion via mechanisms involving SHP and FXR but not FGF15/19 or LXR. These findings implicate BA as regulators of CSAD mRNA via mechanisms shared with CYP7A1.

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KW - Nuclear hormone receptors

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