Urinary excretion of oxidative metabolites of bilirubin in subjects with Gilbert syndrome

Vı́tek, Libor; Kraslova, I.; Muchová, Lucie; Novotný, Ladislav; Yamaguchi, Tokio

doi:10.1111/j.1440-1746.2006.04564.x

Cited by 32 publications

(22 citation statements)

References 37 publications

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“…This individual's records indicated that his serum bilirubin concentrations were at the upper limit of the accepted normal range (2.2-3 g/dl). Nevertheless, this level of plasma bilirubin concentrations corresponds closely to the mean value of 2.7 ± 1.0 observed in 33 Gilbert's syndrome patients versus normal values of 1.0 ± 0.3 in controls (Vitek et al, 2007). Gilbert's syndrome is associated with mutations in one or more genes coding for bilirubin UDP-glucuronyltransferase (UGT) (Teng et al, 2007).…”

Section: Discussionsupporting

confidence: 72%

Kinetics of chloral hydrate and its metabolites in male human volunteers

Merdink¹,

Robison²,

Stevens³

et al. 2008

Toxicology

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Section: Discussionsupporting

confidence: 72%

Kinetics of chloral hydrate and its metabolites in male human volunteers

Merdink¹,

Robison²,

Stevens³

et al. 2008

Toxicology

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“…Bilirubin has also been shown to significantly interfere with the complement system, with all of the possible protective consequences (reviewed in Basiglio et al, 2010). Consistent with this data, several studies have demonstrated a negative relationship between serum bilirubin and C-reactive protein levels (Vítek et al, 2007a; Hwang et al, 2011; Yoshino et al, 2011). In addition, the modulatory effects of bilirubin on T regulatory cell differentiation were recently reported (Rocuts et al, 2010), further underlining the protective role of bilirubin in the pathogenesis of chronic inflammatory as well as in autoimmune conditions.…”

Section: Biological Properties Of Bilirubinsupporting

confidence: 75%

The Role of Bilirubin in Diabetes, Metabolic Syndrome, and Cardiovascular Diseases

Vı́tek¹

2012

Front. Pharmacol.

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270

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Bilirubin belongs to a phylogenetically old superfamily of tetrapyrrolic compounds, which have multiple biological functions. Although for decades bilirubin was believed to be only a waste product of the heme catabolic pathway at best, and a potentially toxic compound at worst; recent data has convincingly demonstrated that mildly elevated serum bilirubin levels are strongly associated with a lower prevalence of oxidative stress-mediated diseases. Indeed, serum bilirubin has been consistently shown to be negatively correlated to cardiovascular diseases (CVD), as well as to CVD-related diseases and risk factors such as arterial hypertension, diabetes mellitus, metabolic syndrome, and obesity. In addition, the clinical data are strongly supported by evidence arising from both in vitro and in vivo experimental studies. This data not only shows the protective effects of bilirubin per se; but additionally, of other products of the heme catabolic pathway such as biliverdin and carbon monoxide, as well as its key enzymes (heme oxygenase and biliverdin reductase); thus, further underlining the biological impacts of this pathway. In this review, detailed information on the experimental and clinical evidence between the heme catabolic pathway and CVD, and those related diseases such as diabetes, metabolic syndrome, and obesity is provided. All of these pathological conditions represent an important threat to human civilization, being the major killers in developed countries, with a steadily increasing prevalence. Thus, it is extremely important to search for novel markers of these diseases, as well as for novel therapeutic modalities to reverse this unfavorable situation. The heme catabolic pathway seems to fulfill the criteria for both diagnostic purposes as well as for potential therapeutical interventions.

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“…18 Vítek et al demonstrated an inverse relationship between serum bilirubin level and urinary excretion of biopyrrins and suggested antioxidative effects of elevated serum bilirubin levels in Gilbert syndrome. 19 Yamamoto et al studied the dynamics of oxidative stress after myocardial ischemia reperfusion in rat models using urinary excretion of biopyrrins and their generation in various organs as oxidative stress markers and suggested that urinary excretion of biopyrrins can serve as a useful marker of systemic oxidative stress after myocardial ischemia -reperfusion. 20 Ueyama et al reported that cardiac and aortic macrophages upregulate HO-1 in response to emotional stress and catecholamine surges as an endogenous defense mechanism against oxidative stress in rat models of takotsubo cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Bilirubin Is Negatively Associated With Hemoglobin A1c Independently of Other Cardiovascular Risk Factors in Apparently Healthy Japanese Men and Women

Oda

Kawai

2011

Circ J

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Background: Serum total bilirubin (TB) is a potent antioxidant and may be a negative risk factor of cardiovascular disease. In non-diabetic adults, hemoglobin A1c (HbA1c), but not fasting plasma glucose, is an independent risk factor of cardiovascular disease. Methods and Results:Linear regression using TB as a dependent variable and cardiovascular risk factors, including HbA1c, as independent variables, linear regression using HbA1c as a dependent variable and other cardiovascular risk factors, including TB, as independent variables, and logistic regression using the highest decile (≥5.4%) of HbA1c as a dependent variable and TB and other cardiovascular risk factors as independent variables were performed for 893 apparently healthy male smokers, 1,607 male nonsmokers, and 1,680 women. The standardized regression coefficient of HbA1c for TB and that of TB for HbA1c was -0.12 (P=0.007) and -0.06 (P=0.02), respectively, in the smokers, -0.20 (P<0.0001) and -0.07 (P<0.0001), respectively, in the nonsmokers, and -0.21 (P< 0.0001) and -0.14 (P<0.0001), respectively, in the women. The odds ratio of 1 SD increment in TB for HbA1c ≥5.4% was not significant in the smokers, 0.67 (P=0.002) in the nonsmokers, and 0.55 (P<0.0001) in the women. Conclusions:Bilirubin was negatively associated with HbA1c independently of other cardiovascular risk factors in apparently healthy Japanese men and women. The association was weak in male smokers. (Circ J 2011; 75: 190 - 195 Bilirubin, A1c, and CVD Methods SubjectsBetween April 2008 and March 2010, 3,401 men and 2,095 women visited Medical Check-up Center, Tachikawa Medical Center, for general health screening. Among them 3,375 men and 2,069 women signed informed consent. Excluding subjects with a history of CVD or who were taking antidiabetic, antihypertensive, or antihyperlipidemic medication from those who gave consent, the resulting 2,500 men and 1,680 women comprised the subjects in the present study, which is part of the study on obesity-related cardiovascular risk factors at Tachikawa Medical Center. Data collected at the first visit were used for subjects who visited 2 or more times. The protocol for the study was approved by the ethics committee at Tachikawa Medical Center and written informed consent was given by each subject.

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Urinary excretion of oxidative metabolites of bilirubin in subjects with Gilbert syndrome

Abstract: An inverse relationship was demonstrated between serum bilirubin level and urinary excretion of biopyrrins, which is presumably due to antioxidative effects of elevated serum bilirubin levels in Gilbert syndrome.

Cited by 32 publications

References 37 publications

Kinetics of chloral hydrate and its metabolites in male human volunteers

Kinetics of chloral hydrate and its metabolites in male human volunteers

The Role of Bilirubin in Diabetes, Metabolic Syndrome, and Cardiovascular Diseases

Bilirubin Is Negatively Associated With Hemoglobin A1c Independently of Other Cardiovascular Risk Factors in Apparently Healthy Japanese Men and Women

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