Glucose induces intestinal human UDP-glucuronosyltransferase (UGT) 1A1 to prevent neonatal hyperbilirubinemia

Scientific Reports
Naoya AoshimaRyoichi Fujiwara

Abstract

Inadequate calorie intake or starvation has been suggested as a cause of neonatal jaundice, which can further cause permanent brain damage, kernicterus. This study experimentally investigated whether additional glucose treatments induce the bilirubin-metabolizing enzyme--UDP-glucuronosyltransferase (UGT) 1A1--to prevent the onset of neonatal hyperbilirubinemia. Neonatal humanized UGT1 (hUGT1) mice physiologically develop jaundice. In this study, UGT1A1 expression levels were determined in the liver and small intestine of neonatal hUGT1 mice that were orally treated with glucose. In the hUGT1 mice, glucose induced UGT1A1 in the small intestine, while it did not affect the expression of UGT1A1 in the liver. UGT1A1 was also induced in the human intestinal Caco-2 cells when the cells were cultured in the presence of glucose. Luciferase assays demonstrated that not only the proximal region (-1300/-7) of the UGT1A1 promoter, but also distal region (-6500/-4050) were responsible for the induction of UGT1A1 in the intestinal cells. Adequate calorie intake would lead to the sufficient expression of UGT1A1 in the small intestine to reduce serum bilirubin levels. Supplemental treatment of newborns with glucose solution can be a convenient...Continue Reading

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Citations

Nov 6, 2015·Phytotherapy Research : PTR·Qian ZhangWei-Ming Wang
Oct 6, 2016·European Journal of Clinical Pharmacology·Ya-Li NieQuan-Cheng Kan
Feb 12, 2019·Xenobiotica; the Fate of Foreign Compounds in Biological Systems·Sabrina JonesRyoichi Fujiwara
May 9, 2015·Drug Metabolism and Disposition : the Biological Fate of Chemicals·Yuki KutsunoRyoichi Fujiwara
Feb 26, 2021·Frontiers in Pharmacology·Ya-Di ZhuGuang-Bo Ge

Methods Mentioned

BETA
PCR

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