Disruption of the Ugt1 Locus in Mice Resembles Human Crigler-Najjar Type I Disease

The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin. Severe unconjugated hyperbilirubinemia in humans that s...

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Published inThe Journal of biological chemistry Vol. 283; no. 12; pp. 7901 - 7911
Main Authors Nguyen, Nghia, Bonzo, Jessica A., Chen, Shujuan, Chouinard, Sarah, Kelner, Michael J., Hardiman, Gary, Bélanger, Alain, Tukey, Robert H.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 21.03.2008
American Society for Biochemistry and Molecular Biology
Subjects
Animals
Bilirubin - blood
Bilirubin - genetics
Crigler-Najjar Syndrome - blood
Crigler-Najjar Syndrome - enzymology
Crigler-Najjar Syndrome - genetics
Crigler-Najjar Syndrome - pathology
Disease Models, Animal
Glucuronosyltransferase - genetics
Glucuronosyltransferase - metabolism
Humans
Liver - enzymology
Liver - pathology
Mice
Mice, Knockout
Quantitative Trait Loci - genetics
Skin Pigmentation - genetics
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Abstract The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin. Severe unconjugated hyperbilirubinemia in humans that suffer from Crigler-Najjar type I disease results from lesions in the UGT1A1 gene and is often fatal. To examine the physiological importance of the Ugt1 locus in mice, this locus was rendered non-functional by interrupting exon 4 to create Ugt1-/- mice. Because UGT1A1 in humans is responsible for 100% of the conjugated bilirubin, it followed that newborn Ugt1-/- mice developed serum levels of unconjugated bilirubin that were 40-60 times higher than Ugt1+/- or wild-type mice. The result of extreme unconjugated bilirubin in Ugt1-/- mice, comparable to the induced levels noted in patients with Crigler-Najjar type 1 disease, is fatal in neonatal Ugt1-/- mice within 2 weeks following birth. The extreme jaundice is present as a phenotype in skin color after 8 h. Neonatal Ugt1-/- mice exhibit no detectable UGT1A-specific RNA, which corresponds to a complete absence of UGT1A proteins in liver microsomes. Conserved glucuronidation activity attributed to the Ugt1 locus can be defined in Ugt1-/- mice, because UGT2-dependent glucuronidation activity is unaffected. Remarkably, the loss of UGT1A functionality in liver results in significant alterations in cellular metabolism as investigated through changes in gene expression. Thus, the loss of UGT1A function in Ugt1-/- mice leads to a metabolic syndrome that can serve as a model to further investigate the toxicities associated with unconjugated bilirubin and the impact of this disease in humans.
AbstractList The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin. Severe unconjugated hyperbilirubinemia in humans that suffer from Crigler-Najjar type I disease results from lesions in the UGT1A1 gene and is often fatal. To examine the physiological importance of the Ugt1 locus in mice, this locus was rendered non-functional by interrupting exon 4 to create Ugt1⁻/⁻ mice. Because UGT1A1 in humans is responsible for 100% of the conjugated bilirubin, it followed that newborn Ugt1⁻/⁻ mice developed serum levels of unconjugated bilirubin that were 40-60 times higher than Ugt1⁺/⁻ or wild-type mice. The result of extreme unconjugated bilirubin in Ugt1⁻/⁻ mice, comparable to the induced levels noted in patients with Crigler-Najjar type 1 disease, is fatal in neonatal Ugt1⁻/⁻ mice within 2 weeks following birth. The extreme jaundice is present as a phenotype in skin color after 8 h. Neonatal Ugt1⁻/⁻ mice exhibit no detectable UGT1A-specific RNA, which corresponds to a complete absence of UGT1A proteins in liver microsomes. Conserved glucuronidation activity attributed to the Ugt1 locus can be defined in Ugt1⁻/⁻ mice, because UGT2-dependent glucuronidation activity is unaffected. Remarkably, the loss of UGT1A functionality in liver results in significant alterations in cellular metabolism as investigated through changes in gene expression. Thus, the loss of UGT1A function in Ugt1⁻/⁻ mice leads to a metabolic syndrome that can serve as a model to further investigate the toxicities associated with unconjugated bilirubin and the impact of this disease in humans.
The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin. Severe unconjugated hyperbilirubinemia in humans that suffer from Crigler-Najjar type I disease results from lesions in the UGT1A1 gene and is often fatal. To examine the physiological importance of the Ugt1 locus in mice, this locus was rendered non-functional by interrupting exon 4 to create Ugt1 super(-/-) mice. Because UGT1A1 in humans is responsible for 100% of the conjugated bilirubin, it followed that newborn Ugt1 super(-/-) mice developed serum levels of unconjugated bilirubin that were 40-60 times higher than Ugt1 super(+/-) or wild-type mice. The result of extreme unconjugated bilirubin in Ugt1 super(-/-) mice, comparable to the induced levels noted in patients with Crigler-Najjar type 1 disease, is fatal in neonatal Ugt1 super(-/-) mice within 2 weeks following birth. The extreme jaundice is present as a phenotype in skin color after 8 h. Neonatal Ugt1 super(-/-) mice exhibit no detectable UGT1A-specific RNA, which corresponds to a complete absence of UGT1A proteins in liver microsomes. Conserved glucuronidation activity attributed to the Ugt1 locus can be defined in Ugt1 super(-/-) mice, because UGT2-dependent glucuronidation activity is unaffected. Remarkably, the loss of UGT1A functionality in liver results in significant alterations in cellular metabolism as investigated through changes in gene expression. Thus, the loss of UGT1A function in Ugt1 super(-/-) mice leads to a metabolic syndrome that can serve as a model to further investigate the toxicities associated with unconjugated bilirubin and the impact of this disease in humans.
The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin. Severe unconjugated hyperbilirubinemia in humans that suffer from Crigler-Najjar type I disease results from lesions in the UGT1A1 gene and is often fatal. To examine the physiological importance of the Ugt1 locus in mice, this locus was rendered non-functional by interrupting exon 4 to create Ugt1(-/-) mice. Because UGT1A1 in humans is responsible for 100% of the conjugated bilirubin, it followed that newborn Ugt1(-/-) mice developed serum levels of unconjugated bilirubin that were 40-60 times higher than Ugt1(+/-) or wild-type mice. The result of extreme unconjugated bilirubin in Ugt1(-/-) mice, comparable to the induced levels noted in patients with Crigler-Najjar type 1 disease, is fatal in neonatal Ugt1(-/-) mice within 2 weeks following birth. The extreme jaundice is present as a phenotype in skin color after 8 h. Neonatal Ugt1(-/-) mice exhibit no detectable UGT1A-specific RNA, which corresponds to a complete absence of UGT1A proteins in liver microsomes. Conserved glucuronidation activity attributed to the Ugt1 locus can be defined in Ugt1(-/-) mice, because UGT2-dependent glucuronidation activity is unaffected. Remarkably, the loss of UGT1A functionality in liver results in significant alterations in cellular metabolism as investigated through changes in gene expression. Thus, the loss of UGT1A function in Ugt1(-/-) mice leads to a metabolic syndrome that can serve as a model to further investigate the toxicities associated with unconjugated bilirubin and the impact of this disease in humans.
The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances such as bile acids, fatty acids, steroids, hormones, neurotransmitters, and bilirubin. Severe unconjugated hyperbilirubinemia in humans that suffer from Crigler-Najjar type I disease results from lesions in the UGT1A1 gene and is often fatal. To examine the physiological importance of the Ugt1 locus in mice, this locus was rendered non-functional by interrupting exon 4 to create Ugt1 -/- mice. Because UGT1A1 in humans is responsible for 100% of the conjugated bilirubin, it followed that newborn Ugt1 -/- mice developed serum levels of unconjugated bilirubin that were 40-60 times higher than Ugt1 +/- or wild-type mice. The result of extreme unconjugated bilirubin in Ugt1 -/- mice, comparable to the induced levels noted in patients with Crigler-Najjar type 1 disease, is fatal in neonatal Ugt1 -/- mice within 2 weeks following birth. The extreme jaundice is present as a phenotype in skin color after 8 h. Neonatal Ugt1 -/- mice exhibit no detectable UGT1A-specific RNA, which corresponds to a complete absence of UGT1A proteins in liver microsomes. Conserved glucuronidation activity attributed to the Ugt1 locus can be defined in Ugt1 -/- mice, because UGT2-dependent glucuronidation activity is unaffected. Remarkably, the loss of UGT1A functionality in liver results in significant alterations in cellular metabolism as investigated through changes in gene expression. Thus, the loss of UGT1A function in Ugt1 -/- mice leads to a metabolic syndrome that can serve as a model to further investigate the toxicities associated with unconjugated bilirubin and the impact of this disease in humans.
Author Chen, Shujuan
Tukey, Robert H.
Hardiman, Gary
Nguyen, Nghia
Bonzo, Jessica A.
Chouinard, Sarah
Bélanger, Alain
Kelner, Michael J.
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  givenname: Jessica A.
  surname: Bonzo
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  organization: Laboratory of Environmental Toxicology, Departments of Chemistry & Biochemistry and Pharmacology, University of California, San Diego, La Jolla, California 92093
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  givenname: Shujuan
  surname: Chen
  fullname: Chen, Shujuan
  organization: Laboratory of Environmental Toxicology, Departments of Chemistry & Biochemistry and Pharmacology, University of California, San Diego, La Jolla, California 92093
– sequence: 4
  givenname: Sarah
  surname: Chouinard
  fullname: Chouinard, Sarah
  organization: Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitare de Québec, Québec G1V 4G2, Canada
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  surname: Hardiman
  fullname: Hardiman, Gary
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  givenname: Alain
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  fullname: Bélanger, Alain
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  surname: Tukey
  fullname: Tukey, Robert H.
  email: rtukey@ucsd.edu
  organization: Laboratory of Environmental Toxicology, Departments of Chemistry & Biochemistry and Pharmacology, University of California, San Diego, La Jolla, California 92093
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SSID ssj0000491
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Snippet The 9 UDP-glucuronosyltranferases (UGTs) encoded by the UGT1 locus in humans are key enzymes in the metabolism of most drugs as well as endogenous substances...
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StartPage 7901
SubjectTerms Animals
Bilirubin - blood
Bilirubin - genetics
Crigler-Najjar Syndrome - blood
Crigler-Najjar Syndrome - enzymology
Crigler-Najjar Syndrome - genetics
Crigler-Najjar Syndrome - pathology
Disease Models, Animal
Glucuronosyltransferase - genetics
Glucuronosyltransferase - metabolism
Humans
Liver - enzymology
Liver - pathology
Mice
Mice, Knockout
Quantitative Trait Loci - genetics
Skin Pigmentation - genetics
Title Disruption of the Ugt1 Locus in Mice Resembles Human Crigler-Najjar Type I Disease
URI https://dx.doi.org/10.1074/jbc.M709244200
http://www.jbc.org/content/283/12/7901.abstract
https://www.ncbi.nlm.nih.gov/pubmed/18180294
https://search.proquest.com/docview/20563990
Volume 283
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