Pathomechanism of neonatal hyperbilirubinemia: the relationship between genetics and nutrition

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860903
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Embryonic/Neonatal medicine
• Research Institution: Yamagata University
• Principal Investigator: SATO Hiroko 山形大学, 医学部, 医員 (10594301)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 高ビリルビン血症 / UGT1A1 / OATP / 母乳栄養

Outline of Final Research Achievements

Neonates have physiologically increased bilirubin production and immature bilirubin metabolism. We previously reported that UGT1A1 211G>A genotype becomes a risk factor under conditions of inadequate feeding. We extended the study to the association of solute-carrier organic anion transporters (SLCOs) polymorphisms with neonatal hyperbilirubinemia. We enrolled infants who were exclusively breastfeeding and classified them into two groups based on the degree of maximal body weight loss. Statistical analysis revealed that maximal body weight loss is the only independent risk factor for the development of neonatal hyperbilirubinemia. UGT1A1, SLCO1B1and SLCO1B3 polymorphisms become risk factors in neonates showing 10% or greater body weight loss during the neonatal period. Inadequate feeding may increase the bilirubin burden and cause apparent hyperbilirubinemia in neonates, who have a polymorphic change in the genes involved in the transport and/or metabolism of bilirubin.

Free Research Field

小児科学