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Upon reactive pathway progression, as in Gilbert\u2019s Syndrome (GS;\n                    <jats:italic>UGT1A1<\/jats:italic>\n                    *28 polymorphism), aggravated health effects have been determined. Based on lower inflammation and improved metabolic health reported for GS, inter-group differences in heme catabolism were explored. Therefore, a case-control study including 120 fasted, healthy, age- and gender matched subjects with\/without GS, was conducted. Genetic expressions of\n                    <jats:italic>HMOX-1<\/jats:italic>\n                    and\n                    <jats:italic>BLVRA<\/jats:italic>\n                    were measured. Additionally participants were genotyped for those polymorphisms that are known (\n                    <jats:italic>UGT1A1<\/jats:italic>\n                    *28) or likely (\n                    <jats:italic>HMOX-1<\/jats:italic>\n                    microsatellites) to impact bilirubinemia. Intracellular interleukins (IL-6, IL-1\u03b2, TNF\u03b1), circulatory C-reactive protein (CRP), serum amyloid A (SAA) and haptoglobin (Hpt) were analysed as inflammatory markers. To assess intracellular heme oxygenase 1 (HO-1) isolated PBMCs were used. In GS vs. C, inflammation markers were significantly decreased. This was supported by an altered heme catabolism, indirectly reflecting in elevated unconjugated bilirubin (UCB; main phenotypic feature of GS) and iron, decreased hemopexin (Hpx) and Hpt and in up-regulated biliverdin reductase (\n                    <jats:italic>BLVRA<\/jats:italic>\n                    ) gene expressions. Moreover,\n                    <jats:italic>HMOX<\/jats:italic>\n                    (GT)\n                    <jats:sub>n<\/jats:sub>\n                    short alleles were non-significantly more prominent in female GS individuals. Herewith, we propose a concept to elucidate why GS individuals encounter lower inflammation, and are thus less prone to oxidative-stress mediated diseases.\n                  <\/jats:p>","DOI":"10.1038\/s41598-017-00933-y","type":"journal-article","created":{"date-parts":[[2017,4,3]],"date-time":"2017-04-03T17:09:31Z","timestamp":1491239371000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Characteristics of the heme catabolic pathway in mild unconjugated hyperbilirubinemia and their associations with inflammation and disease prevention"],"prefix":"10.1038","volume":"7","author":[{"given":"Christine","family":"M\u00f6lzer","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marlies","family":"Wallner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1997-7527","authenticated-orcid":false,"given":"Carina","family":"Kern","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0892-7068","authenticated-orcid":false,"given":"Anela","family":"Tosevska","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ren\u00e9","family":"Zadnikar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Doberer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rodrig","family":"Marculescu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl-Heinz","family":"Wagner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2017,4,7]]},"reference":[{"key":"933_CR1","first-page":"593","volume":"3","author":"P Radu","year":"2001","unstructured":"Radu, P. & Atsmon, J. 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