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Original Paper

Protection from age-related increase in lipid biomarkers and inflammation contributes to cardiovascular protection in Gilbert's syndrome

Marlies Wallner, Rodrig Marculescu, Daniel Doberer, Michael Wolzt, Oswald Wagner, Libor Vitek, Andrew C. Bulmer, Karl-Heinz Wagner
Clinical Science May 10, 2013, 125 (5) 257-264; DOI: 10.1042/CS20120661
Marlies Wallner
Department of Nutritional Sciences, Emerging Field ‘Oxidative Stress and DNA Stability’ and Research Platform ‘Active Ageing’, University of Vienna, Vienna, Austria
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Rodrig Marculescu
Clinical Institute of Laboratory Medicine, Medical University of Vienna, Vienna, Austria
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Daniel Doberer
Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
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Michael Wolzt
Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
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Oswald Wagner
Clinical Institute of Laboratory Medicine, Medical University of Vienna, Vienna, Austria
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Libor Vitek
4th Department of Internal Medicine and Institute of Medical Biochemistry and Laboratory Medicine, Charles University in Prague, Prague, Czech Republic
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Andrew C. Bulmer
Heart Foundation Research Centre, Griffith Health Institute, Griffith University, Southport, Australia
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Karl-Heinz Wagner
Department of Nutritional Sciences, Emerging Field ‘Oxidative Stress and DNA Stability’ and Research Platform ‘Active Ageing’, University of Vienna, Vienna, AustriaHeart Foundation Research Centre, Griffith Health Institute, Griffith University, Southport, Australia
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  • For correspondence: karl-heinz.wagner@univie.ac.at
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Abstract

Recent epidemiological and clinical data show protection from CVD (cardiovascular disease), all-cause mortality and cancer in subjects with GS (Gilbert's syndrome), which is characterized by a mildly elevated blood bilirubin concentration. The established antioxidant effect of bilirubin, however, contributes only in part to this protection. Therefore we investigated whether mildly elevated circulating UCB (unconjugated bilirubin) is associated with altered lipid metabolism. The study was performed on GS and age- and gender-matched healthy subjects (n=59 per group). Full lipoprotein profile, TAG (triacylglycerols), Apo (apolipoprotein)-A1, Apo-B, lipoprotein(a), the subfractions of LDL (low-density lipoprotein) and selected pro-inflammatory mediators were analysed. A hyperbilirubinaemic rodent model (Gunn rats, n=40) was investigated to further support the presented human data. GS subjects had significantly (P<0.05) improved lipid profile with reduced total cholesterol, LDL-C (LDL-cholesterol), TAG, low- and pro-atherogenic LDL subfractions (LDL-1+LDL-2), Apo-B, Apo-B/Apo-A1 ratio and lower IL-6 (interleukin 6) and SAA (serum amyloid A) concentrations (P=0.094). When the control and GS groups were subdivided into younger and older cohorts, older GS subjects demonstrated reduced lipid variables (total cholesterol and LDL-C, TAG and LDL-C subfractions, Apo-B/Apo-A1 ratio; P<0.05; Apo-B: P<0.1) compared with controls. These data were supported by lipid analyses in the rodent model showing that Gunn rat serum had lower total cholesterol (2.29±0.38 compared with 1.27±0.72 mM; P<0.001) and TAG (1.66±0.67 compared with 0.99±0.52 mM; P<0.001) concentrations compared with controls. These findings indicate that the altered lipid profile and the reduced pro-inflammatory status in hyperbilirubinaemic subjects, particularly in the older individuals, probably contribute additionally to the commonly accepted beneficial antioxidant effects of bilirubin in humans.

  • apolipoprotein
  • cardiovascular disease (CVD)
  • Gilbert’s syndrome
  • low-density lipoprotein (LDL)-subfractions
  • lipid metabolism
  • unconjugated bilirubin

Abbreviations: ALP, alkaline phosphatase; ALT, alanine aminotransferase; Apo, apolipoprotein; AST, aspartate aminotransferase; BMI, body mass index; CRP, C-reactive protein; CVD, cardiovascular disease; γ-GT, γ-glutamyl transferase; GS, Gilbert’s syndrome; HDL, high-density lipoprotein; HDL-C, HDL-cholesterol; IDL, intermediate-density lipoprotein; IL, interleukin; LDH, lactate dehydrogenase; LDL, low-density lipoprotein, LDL-C, LDL-cholesterol; NCD, non-communicable disease; SAA, serum amyloid A; TAG, triacylglycerol(s); UCB, unconjugated bilirubin; UGT, uridine diphosphate glucuronosyltransferase; UGT1A1, uridine diphosphate glucuronosyltransferase 1 family, polypeptide A1; VLDL, very-low-density lipoprotein

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September 2013

Volume: 125 Issue: 5

Clinical Science: 125 (5)
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Protection from age-related increase in lipid biomarkers and inflammation contributes to cardiovascular protection in Gilbert's syndrome
Marlies Wallner, Rodrig Marculescu, Daniel Doberer, Michael Wolzt, Oswald Wagner, Libor Vitek, Andrew C. Bulmer, Karl-Heinz Wagner
Clinical Science Sep 2013, 125 (5) 257-264; DOI: 10.1042/CS20120661
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Protection from age-related increase in lipid biomarkers and inflammation contributes to cardiovascular protection in Gilbert's syndrome
Marlies Wallner, Rodrig Marculescu, Daniel Doberer, Michael Wolzt, Oswald Wagner, Libor Vitek, Andrew C. Bulmer, Karl-Heinz Wagner
Clinical Science Sep 2013, 125 (5) 257-264; DOI: 10.1042/CS20120661

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Keywords

apolipoprotein
cardiovascular disease (CVD)
Gilbert’s syndrome
low-density lipoprotein (LDL)-subfractions
lipid metabolism
unconjugated bilirubin

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