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Sci Rep. 2016 Mar 1;6:22300. doi: 10.1038/srep22300.

Longer telomeres in chronic, moderate, unconjugated hyperbilirubinaemia: insights from a human study on Gilbert's Syndrome.

Author information

1
Research Platform Active Ageing, University of Vienna, Althanstrasse 14, 1090, Vienna, Austria.
2
Department of Nutritional Sciences, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
3
Institute of Dietetics and Nutrition, University of Applied Sciences, FH JOANNEUM, Alte Poststraße 149, 8020 Graz, Austria.
4
Institute of Pharmacology, Medical University of Vienna, Waehringer Str. 13a, 1090 Vienna, Austria.
5
Clinical Institute of Laboratory Medicine, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
6
Department of Clinical Pharmacology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
7
Department of Ecogenomics and Systems Biology, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
8
Vienna Metabolomics Center (VIME), University of Vienna, Althanstrasse 14, 1090, Vienna, Austria.

Abstract

Bilirubin (BR) is a natural endogenous compound with a potent bioactivity. Gilbert's Syndrome (GS) is a benign hereditary condition of increased unconjugated bilirubin (UCB) in serum and serves as a convenient model for studying the effects of BR in humans. In absence of liver disease, increased UCB levels are inversely associated to all-cause mortality risk, especially from cardiovascular diseases (CVDs). On the other hand, telomere malfunction is linked to a higher risk of CVDs. To our knowledge, there is no data on whether UCB is linked to telomere length in healthy or diseased individuals In the present study we have observed a relationship between mildly increased serum UCB and telomere length. We used an in vivo approach, assessing telomere length in PBMCs from individuals with GS (n = 60) and matched healthy controls (n = 60). An occurrence of longer telomeres was observed in male individuals chronically exposed to increased UCB, as well as in Gunn rats, an animal model of unconjugated hyperbilirubinaemia. Previously identified differences in immunomodulation and redox parameters in individuals with GS, such as IL-6, IL-1β and ferric reducing ability of plasma, were confirmed and proposed as possible contributors to the occurrence of longer telomeres in GS.

PMID:
26926838
PMCID:
PMC4772088
DOI:
10.1038/srep22300
[Indexed for MEDLINE]
Free PMC Article

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