Abstract
Bilirubin is an important antioxidant and a modulator of biological functions. However, most of the protection against oxidative stress was shown in vitro or ex vivo. The aim of this case-control study was to investigate whether subjects with Gilbert’s syndrome (GS) experience different levels of lipid and protein oxidation (as well as differences in oxidative stress related markers) compared to healthy controls. GS subjects (n = 119) demonstrated higher serum levels of unconjugated bilirubin (p < 0.001), a lower BMI (p < 0.001), 37% higher antioxidant potential assessed as ferric reducing ability potential (p < 0.001), higher advanced oxidation protein products (p < 0.01) andlower apolipoprotein B (p < 0.05), hs-C-reactive protein (p < 0.05), interleukin 6 (p < 0.001) and interleukin 1 beta (p < 0.05) values compared to healthy controls (n = 119). Furthermore, the resting heart rate was significantly lower in the GS group (p < 0.05). Stronger protective effects for GS subjects were demonstrated in the older subgroup (n = 104, average age 50 years) compared to those of the younger group (n = 134, average age 27 years). Although not all markers related to oxidative stress were different between the groups (e.g., malondialdehyde, homocysteine, oxLDL, and myeloperoxidase; p > 0.05), the observed differences contribute to the explanation of why GS serves as an important protector in the pathogenesis of metabolic, oxidative stress related diseases.
Highlights
Glucuronosyltransferase 1A1 (UGT1A1) gene leading to a reduced conjugating activity of this enzyme, which is phenotypically resulting in a mild increase in unconjugated bilirubin (UCB) [2]
Since body weight and composition is changing with age [36] the Gilbert’s syndrome (GS) phenotype with a lower body weight in the 4th to 6th decade of life compared to controls, significantly contribute to the reduced risk of cardiovascular disease (CVD) and all-cause mortality in this population group [37]
We investigated the oxidation products MDA, oxidized LDL (oxLDL), advanced oxidation protein products (AOPP), the total antioxidant capacity (FRAP), antioxidants such as GSH or uric acid, inflammatory markers
Summary
Known as Gilbert’s syndrome (GS), is prevalent in. 5–10% of the general population, up to 20% in some areas such as the Middle East [1]. This condition is based on various underlying promoter polymorphisms in the UDP glucuronosyltransferase 1A1 (UGT1A1) gene leading to a reduced conjugating activity of this enzyme, which is phenotypically resulting in a mild increase in unconjugated bilirubin (UCB) (total bilirubin >17.1 μM/L) [2]. Individuals with GS are protected from coronary artery disease (CAD), ischemic heart disease, atherosclerosis, all-cause mortality, and some cancers (e.g., lung cancer [3,4,5,6,7,8]).
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