Open AccessCholine supplementation prevents the effects of bilirubin on cerebellar-mediated behavior in choline-restricted Gunn rat pups
Author(s) -
Jaylyn Waddell,
Nicholas Rickman,
Min He,
Ningfeng Tang,
Cynthia F. Bearer
Publication year - 2020
Publication title -
pediatric research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.056
H-Index - 150
eISSN - 1530-0447
pISSN - 0031-3998
DOI - 10.1038/s41390-020-01187-7
Subject(s) - choline , bilirubin , medicine , endocrinology , neuroprotection , neurotoxicity , physiology , toxicity
Bilirubin is produced by the breakdown of hemoglobin and is normally catabolized and excreted. Neurotoxic accumulation of serum bilirubin often occurs in premature infants. The homozygous Gunn rat lacks uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1), the enzyme needed to biotransform bilirubin. This rodent model of hyperbilirubinemia emulates many aspects of bilirubin toxicity observed in the human infant. We demonstrate that choline supplementation in early postnatal development is neuroprotective in the choline-restricted Gunn rat, when hyperbilirubinemia is induced on postnatal day 5.