Polymorphic Human Sulfotransferase 2A1 Mediates the Formation of 25-Hydroxyvitamin D3-3-O-Sulfate, a Major Circulating Vitamin D Metabolite in Humans

Metabolism of 25-hydroxyvitamin D3 (25OHD3) plays a central role in regulating the biologic effects of vitamin D in the body. Although cytochrome P450-dependent hydroxylation of 25OHD3 has been extensively investigated, limited information is available on the conjugation of 25OHD3 In this study, we...

Celý popis

Uloženo v:
Podrobná bibliografie
Vydáno v:Drug metabolism and disposition Ročník 46; číslo 4; s. 367
Hlavní autoři: Wong, Timothy, Wang, Zhican, Chapron, Brian D, Suzuki, Mizuki, Claw, Katrina G, Gao, Chunying, Foti, Robert S, Prasad, Bhagwat, Chapron, Alenka, Calamia, Justina, Chaudhry, Amarjit, Schuetz, Erin G, Horst, Ronald L, Mao, Qingcheng, de Boer, Ian H, Thornton, Timothy A, Thummel, Kenneth E
Médium: Journal Article
Jazyk:angličtina
Vydáno: 01.04.2018
ISSN:1521-009X, 1521-009X
On-line přístup:Zjistit podrobnosti o přístupu
Tagy: Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
Abstract Metabolism of 25-hydroxyvitamin D3 (25OHD3) plays a central role in regulating the biologic effects of vitamin D in the body. Although cytochrome P450-dependent hydroxylation of 25OHD3 has been extensively investigated, limited information is available on the conjugation of 25OHD3 In this study, we report that 25OHD3 is selectively conjugated to 25OHD3-3-O-sulfate by human sulfotransferase 2A1 (SULT2A1) and that the liver is a primary site of metabolite formation. At a low (50 nM) concentration of 25OHD3, 25OHD3-3-O-sulfate was the most abundant metabolite, with an intrinsic clearance approximately 8-fold higher than the next most efficient metabolic route. In addition, 25OHD3 sulfonation was not inducible by the potent human pregnane X receptor agonist, rifampicin. The 25OHD3 sulfonation rates in a bank of 258 different human liver cytosols were highly variable but correlated with the rates of dehydroepiandrosterone sulfonation. Further analysis revealed a significant association between a common single nucleotide variant within intron 1 of SULT2A1 (rs296361; minor allele frequency = 15% in whites) and liver cytosolic SULT2A1 content as well as 25OHD3-3-O-sulfate formation rate, suggesting that variation in the SULT2A1 gene contributes importantly to interindividual differences in vitamin D homeostasis. Finally, 25OHD3-3-O-sulfate exhibited high affinity for the vitamin D binding protein and was detectable in human plasma and bile but not in urine samples. Thus, circulating concentrations of 25OHD3-3-O-sulfate appear to be protected from rapid renal elimination, raising the possibility that the sulfate metabolite may serve as a reservoir of 25OHD3 in vivo, and contribute indirectly to the biologic effects of vitamin D.Metabolism of 25-hydroxyvitamin D3 (25OHD3) plays a central role in regulating the biologic effects of vitamin D in the body. Although cytochrome P450-dependent hydroxylation of 25OHD3 has been extensively investigated, limited information is available on the conjugation of 25OHD3 In this study, we report that 25OHD3 is selectively conjugated to 25OHD3-3-O-sulfate by human sulfotransferase 2A1 (SULT2A1) and that the liver is a primary site of metabolite formation. At a low (50 nM) concentration of 25OHD3, 25OHD3-3-O-sulfate was the most abundant metabolite, with an intrinsic clearance approximately 8-fold higher than the next most efficient metabolic route. In addition, 25OHD3 sulfonation was not inducible by the potent human pregnane X receptor agonist, rifampicin. The 25OHD3 sulfonation rates in a bank of 258 different human liver cytosols were highly variable but correlated with the rates of dehydroepiandrosterone sulfonation. Further analysis revealed a significant association between a common single nucleotide variant within intron 1 of SULT2A1 (rs296361; minor allele frequency = 15% in whites) and liver cytosolic SULT2A1 content as well as 25OHD3-3-O-sulfate formation rate, suggesting that variation in the SULT2A1 gene contributes importantly to interindividual differences in vitamin D homeostasis. Finally, 25OHD3-3-O-sulfate exhibited high affinity for the vitamin D binding protein and was detectable in human plasma and bile but not in urine samples. Thus, circulating concentrations of 25OHD3-3-O-sulfate appear to be protected from rapid renal elimination, raising the possibility that the sulfate metabolite may serve as a reservoir of 25OHD3 in vivo, and contribute indirectly to the biologic effects of vitamin D.
AbstractList Metabolism of 25-hydroxyvitamin D3 (25OHD3) plays a central role in regulating the biologic effects of vitamin D in the body. Although cytochrome P450-dependent hydroxylation of 25OHD3 has been extensively investigated, limited information is available on the conjugation of 25OHD3 In this study, we report that 25OHD3 is selectively conjugated to 25OHD3-3-O-sulfate by human sulfotransferase 2A1 (SULT2A1) and that the liver is a primary site of metabolite formation. At a low (50 nM) concentration of 25OHD3, 25OHD3-3-O-sulfate was the most abundant metabolite, with an intrinsic clearance approximately 8-fold higher than the next most efficient metabolic route. In addition, 25OHD3 sulfonation was not inducible by the potent human pregnane X receptor agonist, rifampicin. The 25OHD3 sulfonation rates in a bank of 258 different human liver cytosols were highly variable but correlated with the rates of dehydroepiandrosterone sulfonation. Further analysis revealed a significant association between a common single nucleotide variant within intron 1 of SULT2A1 (rs296361; minor allele frequency = 15% in whites) and liver cytosolic SULT2A1 content as well as 25OHD3-3-O-sulfate formation rate, suggesting that variation in the SULT2A1 gene contributes importantly to interindividual differences in vitamin D homeostasis. Finally, 25OHD3-3-O-sulfate exhibited high affinity for the vitamin D binding protein and was detectable in human plasma and bile but not in urine samples. Thus, circulating concentrations of 25OHD3-3-O-sulfate appear to be protected from rapid renal elimination, raising the possibility that the sulfate metabolite may serve as a reservoir of 25OHD3 in vivo, and contribute indirectly to the biologic effects of vitamin D.Metabolism of 25-hydroxyvitamin D3 (25OHD3) plays a central role in regulating the biologic effects of vitamin D in the body. Although cytochrome P450-dependent hydroxylation of 25OHD3 has been extensively investigated, limited information is available on the conjugation of 25OHD3 In this study, we report that 25OHD3 is selectively conjugated to 25OHD3-3-O-sulfate by human sulfotransferase 2A1 (SULT2A1) and that the liver is a primary site of metabolite formation. At a low (50 nM) concentration of 25OHD3, 25OHD3-3-O-sulfate was the most abundant metabolite, with an intrinsic clearance approximately 8-fold higher than the next most efficient metabolic route. In addition, 25OHD3 sulfonation was not inducible by the potent human pregnane X receptor agonist, rifampicin. The 25OHD3 sulfonation rates in a bank of 258 different human liver cytosols were highly variable but correlated with the rates of dehydroepiandrosterone sulfonation. Further analysis revealed a significant association between a common single nucleotide variant within intron 1 of SULT2A1 (rs296361; minor allele frequency = 15% in whites) and liver cytosolic SULT2A1 content as well as 25OHD3-3-O-sulfate formation rate, suggesting that variation in the SULT2A1 gene contributes importantly to interindividual differences in vitamin D homeostasis. Finally, 25OHD3-3-O-sulfate exhibited high affinity for the vitamin D binding protein and was detectable in human plasma and bile but not in urine samples. Thus, circulating concentrations of 25OHD3-3-O-sulfate appear to be protected from rapid renal elimination, raising the possibility that the sulfate metabolite may serve as a reservoir of 25OHD3 in vivo, and contribute indirectly to the biologic effects of vitamin D.
Author Foti, Robert S
Chaudhry, Amarjit
Mao, Qingcheng
de Boer, Ian H
Prasad, Bhagwat
Gao, Chunying
Horst, Ronald L
Wang, Zhican
Claw, Katrina G
Chapron, Alenka
Schuetz, Erin G
Suzuki, Mizuki
Calamia, Justina
Thummel, Kenneth E
Thornton, Timothy A
Chapron, Brian D
Wong, Timothy
Author_xml – sequence: 1
  givenname: Timothy
  surname: Wong
  fullname: Wong, Timothy
– sequence: 2
  givenname: Zhican
  surname: Wang
  fullname: Wang, Zhican
– sequence: 3
  givenname: Brian D
  surname: Chapron
  fullname: Chapron, Brian D
– sequence: 4
  givenname: Mizuki
  surname: Suzuki
  fullname: Suzuki, Mizuki
– sequence: 5
  givenname: Katrina G
  surname: Claw
  fullname: Claw, Katrina G
– sequence: 6
  givenname: Chunying
  surname: Gao
  fullname: Gao, Chunying
– sequence: 7
  givenname: Robert S
  surname: Foti
  fullname: Foti, Robert S
– sequence: 8
  givenname: Bhagwat
  surname: Prasad
  fullname: Prasad, Bhagwat
– sequence: 9
  givenname: Alenka
  surname: Chapron
  fullname: Chapron, Alenka
– sequence: 10
  givenname: Justina
  surname: Calamia
  fullname: Calamia, Justina
– sequence: 11
  givenname: Amarjit
  surname: Chaudhry
  fullname: Chaudhry, Amarjit
– sequence: 12
  givenname: Erin G
  surname: Schuetz
  fullname: Schuetz, Erin G
– sequence: 13
  givenname: Ronald L
  surname: Horst
  fullname: Horst, Ronald L
– sequence: 14
  givenname: Qingcheng
  surname: Mao
  fullname: Mao, Qingcheng
– sequence: 15
  givenname: Ian H
  surname: de Boer
  fullname: de Boer, Ian H
– sequence: 16
  givenname: Timothy A
  surname: Thornton
  fullname: Thornton, Timothy A
– sequence: 17
  givenname: Kenneth E
  surname: Thummel
  fullname: Thummel, Kenneth E
BookMark eNpNjl1LwzAYhYNMcJveep1LL8zMm6ZNezmmc8LGBD_wbsQ2cRltMpNU7A_x_1q_QHjhnAPnPLwjNLDOKoROgU4AGL-omqo3YkJFzll-gIaQMiCUFk-Df_4IjULYUQqcJ8UQfdy6umuc329NiRdtIy2-a2vtopc2aOVlUJhNAa9UZWRUAcetwnPnGxmNs9hpzFKy6Crv3rs3E2VjLL5MSELW5IvTT86xxCu5cx7PjC_buh_aF_z41-3JUT672kSF-_z9QjhGh1rWQZ386hg9zK_uZwuyXF_fzKZLUvKcRVIJXjGgIlGQCa6ZKPsrOGe8zIErQbO0ylNNU6F4lkKipaJaAEhOBWSaszE6--HuvXttVYibxoRS1bW0yrVhA0VeZDRJipx9AoSZa1o
CitedBy_id crossref_primary_10_1016_j_jsbmb_2021_106047
crossref_primary_10_1007_s12013_020_00938_x
crossref_primary_10_1016_j_jmsacl_2022_04_001
crossref_primary_10_1016_j_exger_2025_112836
crossref_primary_10_1016_j_jsbmb_2019_105516
crossref_primary_10_1042_EBC20240034
crossref_primary_10_1016_j_jsbmb_2023_106367
crossref_primary_10_1016_j_steroids_2020_108695
crossref_primary_10_33176_AACB_20_00006
crossref_primary_10_1042_EBC20240030
crossref_primary_10_1016_j_ajhg_2020_01_017
crossref_primary_10_1016_j_jsbmb_2022_106229
crossref_primary_10_1016_j_jsbmb_2018_07_012
crossref_primary_10_1210_jc_2019_00207
crossref_primary_10_1681_ASN_2020050625
crossref_primary_10_1016_j_steroids_2021_108812
crossref_primary_10_1124_dmd_119_086462
crossref_primary_10_1210_clinem_dgab708
crossref_primary_10_1124_pharmrev_121_000449
crossref_primary_10_1093_pnasnexus_pgac063
crossref_primary_10_1007_s44211_023_00350_4
crossref_primary_10_1016_j_jsbmb_2022_106133
crossref_primary_10_3390_nu13061758
crossref_primary_10_1124_dmd_117_078881
crossref_primary_10_1016_j_jsbmb_2023_106332
crossref_primary_10_3390_nu14204408
crossref_primary_10_1016_j_clnu_2024_07_008
crossref_primary_10_1210_clinem_dgaf025
crossref_primary_10_1016_j_jpba_2023_115958
crossref_primary_10_1038_s41467_020_15421_7
crossref_primary_10_1042_EBC20230101
crossref_primary_10_1002_jbmr_3884
crossref_primary_10_1002_bmc_4538
crossref_primary_10_1002_cbf_3421
crossref_primary_10_1124_dmd_121_000609
crossref_primary_10_1002_jcph_1709
crossref_primary_10_1016_j_bcp_2018_07_015
crossref_primary_10_1016_j_jbc_2021_100668
ContentType Journal Article
Copyright Copyright © 2018 by The American Society for Pharmacology and Experimental Therapeutics.
Copyright_xml – notice: Copyright © 2018 by The American Society for Pharmacology and Experimental Therapeutics.
DBID 7X8
DOI 10.1124/dmd.117.078428
DatabaseName MEDLINE - Academic
DatabaseTitle MEDLINE - Academic
DatabaseTitleList MEDLINE - Academic
Database_xml – sequence: 1
  dbid: 7X8
  name: MEDLINE - Academic
  url: https://search.proquest.com/medline
  sourceTypes: Aggregation Database
DeliveryMethod no_fulltext_linktorsrc
Discipline Pharmacy, Therapeutics, & Pharmacology
EISSN 1521-009X
GroupedDBID ---
0R~
18M
2WC
4.4
53G
5GY
5RE
5VS
7X8
AALRI
AAXUO
ABJNI
ABSQV
ACGFO
ACGFS
ACIWK
ACPRK
ADBBV
AENEX
AFRAH
ALMA_UNASSIGNED_HOLDINGS
BAWUL
BTFSW
CS3
DIK
DU5
E3Z
EBS
EJD
F5P
F9R
FDB
GX1
H13
HZ~
IH2
INIJC
KQ8
LSO
M41
O9-
OK1
P2P
R0Z
RHI
ROL
RPT
SJN
TR2
W8F
WH7
WOQ
YHG
~KM
ID FETCH-LOGICAL-c482t-d74d21073e1674f27c27c94424c814e7065d85f057e46513fae0f711a40716f42
IEDL.DBID 7X8
ISICitedReferencesCount 40
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000426966600005&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1521-009X
IngestDate Fri Sep 05 12:16:53 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 4
Language English
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c482t-d74d21073e1674f27c27c94424c814e7065d85f057e46513fae0f711a40716f42
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
OpenAccessLink https://dmd.aspetjournals.org/content/dmd/46/4/367.full.pdf
PQID 1989603398
PQPubID 23479
ParticipantIDs proquest_miscellaneous_1989603398
PublicationCentury 2000
PublicationDate 20180401
PublicationDateYYYYMMDD 2018-04-01
PublicationDate_xml – month: 04
  year: 2018
  text: 20180401
  day: 01
PublicationDecade 2010
PublicationTitle Drug metabolism and disposition
PublicationYear 2018
SSID ssj0014439
Score 2.4373295
Snippet Metabolism of 25-hydroxyvitamin D3 (25OHD3) plays a central role in regulating the biologic effects of vitamin D in the body. Although cytochrome...
SourceID proquest
SourceType Aggregation Database
StartPage 367
Title Polymorphic Human Sulfotransferase 2A1 Mediates the Formation of 25-Hydroxyvitamin D3-3-O-Sulfate, a Major Circulating Vitamin D Metabolite in Humans
URI https://www.proquest.com/docview/1989603398
Volume 46
WOSCitedRecordID wos000426966600005&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText
inHoldings 1
isFullTextHit
isPrint
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1JSwMxFA5uBy_u4s4TxFOjnUnaZE4iavHgUnChN8lkkZF2Rjuj0B_i__UlndKDF0GYSyAJYfLy3pe85SPkiDWti1I8aSkqYIoW2tJEMk2NitpJywjt0lBd_0bc3cleL-nWD25lHVY50YlBUZtC-zfyUx_b024ylsiz9w_qWaO8d7Wm0Jgl8wyhjJdq0Zt6ETgPTGLeRFHEEr26aCOatFMzMN5feYIWksfylyIO1qWz_N91rZClGlfC-VgQVsmMzdfIcXdcmHrUgMdpnlXZgGPoTktWj9bJd7fojwYF_vNMQ3jXh4fPviuqAGtxZGkhPo_gNhB72BIQNkJnkvcIhYO4Ra9HxsfEfGWVGmQ5XDLK6D318-CQBii4VW_FEC6yoQ6cYfkrPE_64swViqNPiAZshyWUG-Spc_V4cU1rwgaquYwragQ3eIUUzPrcBhcLjV_Cecy1jLj1HlUjWw4hovUU7Mwp23QiipS_VbYdjzfJXF7kdouAtiJSsUMA1VZcpkzyVLJUyLSVeMTa3CaHk-14wQPhvRwqt8Vn-TLdkJ0_9NkliwiB5DgWZ4_MOzz0dp8s6K8qK4cHQZ5-ANcy1Vw
linkProvider ProQuest
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Polymorphic+Human+Sulfotransferase+2A1+Mediates+the+Formation+of+25-Hydroxyvitamin+D3-3-O-Sulfate%2C+a+Major+Circulating+Vitamin+D+Metabolite+in+Humans&rft.jtitle=Drug+metabolism+and+disposition&rft.au=Wong%2C+Timothy&rft.au=Wang%2C+Zhican&rft.au=Chapron%2C+Brian+D&rft.au=Suzuki%2C+Mizuki&rft.date=2018-04-01&rft.issn=1521-009X&rft.eissn=1521-009X&rft.volume=46&rft.issue=4&rft.spage=367&rft_id=info:doi/10.1124%2Fdmd.117.078428&rft.externalDBID=NO_FULL_TEXT
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1521-009X&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1521-009X&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1521-009X&client=summon