ArticleBMC genetics2015
Serum bilirubin concentration is modified by UGT1A1 haplotypes and influences risk of type-2 diabetes in the Norfolk Island genetic isolate.
Article in BMC genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Revealing genetic foundations underlying cardiometabolic traits: integrating twin and GWAS data in Asian populations.International journal of obesity (2005) · 2026Article
- Total mixed ration enhances nutrient digestibility, blood biochemical parameters and faecal microbial diversity in horses.BMC veterinary research · 2025Article
- Bidirectional Causal Associations Between Endogenous/Exogenous Antioxidant Levels and Risks of Type 1 and Type 2 Diabetes Mellitus and Three Complications.Food science & nutrition · 2025Article
- Circulating Bilirubin Levels, but Not Their Genetic Determinants, Are Inversely Associated with Steatotic Liver Disease in Adolescents.International journal of molecular sciences · 2025Article
- Genetic determinants of serum bilirubin using inferred native American gene variants in Chilean adolescents.Frontiers in genetics · 2024Article
- Suppressing Hepatic UGT1A1 Increases Plasma Bilirubin, Lowers Plasma Urobilin, Reorganizes Kinase Signaling Pathways and Lipid Species and Improves Fatty Liver Disease.Biomolecules · 2023Article
- Low Antioxidant Status of Serum Uric Acid, Bilirubin, Albumin, and Creatinine in Patients With Benign Paroxysmal Positional Vertigo.Frontiers in neurology · 2020Article
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLocated in the Pacific Ocean between Australia and New Zealand, the unique population isolate of Norfolk Island has been shown to exhibit increased prevalence of metabolic disorders (type-2 diabetes, cardiovascular disease) compared to mainland Australia. We investigated this well-established genetic isolate, utilising its unique genomic structure to increase the ability to detect related genetic markers. A pedigree-based genome-wide association study of 16 routinely collected blood-based clinical traits in 382 Norfolk Island individuals was performed.
resultsA striking association peak was located at chromosome 2q37.1 for both total bilirubin and direct bilirubin, with 29 SNPs reaching statistical significance (P < 1.84 × 10(-7)). Strong linkage disequilibrium was observed across a 200 kb region spanning the UDP-glucuronosyltransferase family, including UGT1A1, an enzyme known to metabolise bilirubin. Given the epidemiological literature suggesting negative association between CVD-risk and serum bilirubin we further explored potential associations using stepwise multivariate regression, revealing significant association between direct bilirubin concentration and type-2 diabetes risk. In the Norfolk Island cohort increased direct bilirubin was associated with a 28% reduction in type-2 diabetes risk (OR: 0.72, 95% CI: 0.57-0.91, P = 0.005). When adjusted for genotypic effects the overall model was validated, with the adjusted model predicting a 30% reduction in type-2 diabetes risk with increasing direct bilirubin concentrations (OR: 0.70, 95% CI: 0.53-0.89, P = 0.0001).
conclusionsIn summary, a pedigree-based GWAS of blood-based clinical traits in the Norfolk Island population has identified variants within the UDPGT family directly associated with serum bilirubin levels, which is in turn implicated with reduced risk of developing type-2 diabetes within this population.
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