Stercobilinogen

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Stercobilinogen
Stercobilinogen.png
Names
IUPAC name
3-[2-{{#parsoidfragment:0}}3-(2-carboxyethyl)-5-{{#parsoidfragment:1}}(2S,3R,4R)-4-ethyl-3-methyl-5-oxopyrrolidin-2-yl]methyl]-4-methyl-1H-pyrrol-2-yl]methyl]-5-{{#parsoidfragment:2}}(2S,3R,4R)-3-ethyl-4-methyl-5-oxopyrrolidin-2-yl]methyl]-4-methyl-1H-pyrrol-3-yl]propanoic acid
Other names
Fecal urobilinogen
Identifiers
3D model (JSmol)
ChEBI
ChemSpider
MeSH Stercobilinogen
PubChem CID
UNII
  • InChI=1S/C33H48N4O6/c1-7-20-19(6)32(42)37-27(20)14-25-18(5)23(10-12-31(40)41)29(35-25)15-28-22(9-11-30(38)39)17(4)24(34-28)13-26-16(3)21(8-2)33(43)36-26/h16,19-21,26-27,34-35H,7-15H2,1-6H3,(H,36,43)(H,37,42)(H,38,39)(H,40,41)/t16-,19-,20-,21-,26+,27+/m1/s1 X mark.svgN
    Key: VKGRRZVYCXLHII-OLFWPHQKSA-N X mark.svgN
  • InChI=1/C33H48N4O6/c1-7-20-19(6)32(42)37-27(20)14-25-18(5)23(10-12-31(40)41)29(35-25)15-28-22(9-11-30(38)39)17(4)24(34-28)13-26-16(3)21(8-2)33(43)36-26/h16,19-21,26-27,34-35H,7-15H2,1-6H3,(H,36,43)(H,37,42)(H,38,39)(H,40,41)/t16-,19-,20-,21-,26+,27+/m1/s1
    Key: VKGRRZVYCXLHII-OLFWPHQKBU
  • CC[C@@H]1[C@H](C(=O)N[C@H]1CC2=C(C(=C(N2)CC3=C(C(=C(N3)C[C@H]4[C@@H]([C@H](C(=O)N4)CC)C)C)CCC(=O)O)CCC(=O)O)C)C
Properties
C33H48N4O6
Molar mass 596.769 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
X mark.svgN  verify  (what is  Yes check.svgYX mark.svgN ?)

Stercobilinogen (fecal urobilinogen) is an intermediate product of hemoglobin degradation, produced by the bacterial metabolism of bilirubin in the intestine. [1] [2] [3] Stercobilinogen is converted by oxidation to stercobilin, which is responsible for the brown color of feces. [4] [5]

Contents

Bilirubin is a pigment that results from the breakdown of the heme portion of hemoglobin. The liver conjugates bilirubin, making it water-soluble; and the conjugated form is then excreted in urine as urobilinogen and in the feces as stercobilinogen. Urobilinogen / stercobilinogen is colourless and is further oxidised to stercobilin which imparts colour to feces. Darkening of feces upon standing in air is due to the oxidation of residual urobilinogens to urobilins. In the intestine, bilirubin is converted by bacteria to stercobilinogen. Stercobilinogen is absorbed and excreted by either the liver or the kidney.

Stercobilinogen and its derivatives play an important role in the diagnosis of liver and biliary diseases and serve as markers for disorders of bilirubin metabolism and for changes in the intestinal microbiome.

Biochemistry

During metabolism, bilirubin, which is formed in the liver and excreted via the bile into the small intestine, is first reduced by intestinal bacteria to urobilinogen, which is then converted to stercobilinogen. Anaerobic bacteria of the genera Clostridia , Bacteroides , and Eubacteriales , whose bilirubin reductases catalyze intermediates such as mesobilirubinogen and D-urobilinogen, are primarily responsible for this conversion. [6] Sterkobilinogen wird schließlich durch Oxidation zu Sterkobilin umgewandelt. [3]

About 80 percent of the stercobilin formed is excreted in the stool, while the remaining 20 percent is reabsorbed and returned to the liver via the enterohepatic circulation or excreted via the kidney after oxidation to urobilin. [3] [7] Stercobilinogen thus represents a central link between bilirubin and urobilin metabolism.

Clinical significance

The concentration of stercobilinogen in the intestine and urine is an important diagnostic marker. In diseases such as bile duct obstruction or cholestasis, the formation of stercobilinogen is reduced, resulting in pale, clay-colored stools. [8] In contrast, increased stercobilinogen and urobilinogen levels occur in hemolysis, hepatitis, or increased erythrocyte degradation. [9] Changes in stercobilinogen concentration can also indicate bacterial dysbiosis or dysfunctions in bilirubin metabolism. [6]

Stercobilinogen is classically detected by means of the Ehrlich aldehyde reaction, in which a red azo dye is formed. [10] In modern diagnostics, high-performance liquid chromatography (HPLC) and mass spectrometry are increasingly used to differentiate structurally related bilinogens such as urobilinogen, mesobilinogen, and stercobilinogen. [3] [11]

Research results

Recent studies (as of November 2025) have identified the bacterial enzyme bilirubin reductase as crucial for the reduction of bilirubin to urobilinogen and thus for the formation of stercobilinogen. [12] Studies in mouse models show that stercobilinogen and its oxidation products exhibit proinflammatory properties. These substances activate genes such as TNFα, IL1, IL-6, and COX-2, promote inflammatory processes, and are associated with metabolic diseases such as obesity and diabetes, as well as neurological disorders such as autism. [13]

The underlying mechanisms presumably involve activation of TLR4-mediated signaling pathways and the NF-κB cascade, which stimulates immune cells and induces the release of inflammatory cytokines. In parallel, microbiome-associated studies have correlated elevated stercobilinogen levels with reduced bacterial diversity and a shift in the Firmicutes/Bacteroidetes ratio. [3] [14] [15]

Application

Stercobilinogen is increasingly being investigated as a biomarker in clinical diagnostics and translational research. It can be detected in urine and serves as a non-invasive supplement to imaging diagnostics in certain liver and tumor diseases. [16] In addition, stercobilinogen derivative profiles are being studied as markers for the early detection of colorectal carcinoma, for monitoring the progression of chronic inflammatory bowel diseases, and for assessing intestinal barrier integrity. [3] [17]

Literature

References

  1. ↑ Harpers Illustrated Biochemistry (28th ed.).
  2. ↑ Harrison’s Principles of Internal Medicine (20th ed.).
  3. 1 2 3 4 5 6 Toh, E. C. et al. (2024). Microbial bilirubin metabolism and host inflammation: Stercobilinogen as a gut-liver axis signaling molecule. Frontiers in Microbiology, 15, 14219.
  4. ↑ "Chemie und Klinik der Bilirubinreduktionsprodukte Urobilin und Sterkoblin.", Archives of Pediatrics & Adolescent Medicine, vol. 87, no. 1, p. 122, 1954-01-01, doi:10.1001/archpedi.1954.02050090122019, ISSN   1072-4710
  5. ↑ Stercobilinogen, drugs.com
  6. 1 2 Brantley Hall, Sophia Levy, Keith Dufault-Thompson, Gabriela Arp, Aoshu Zhong, Glory Minabou Ndjite, Ashley Weiss, Domenick Braccia, Conor Jenkins, Maggie R. Grant, Stephenie Abeysinghe, Yiyan Yang, Madison D. Jermain, Chih Hao Wu, Bing Ma, Xiaofang Jiang (January 2024), "BilR is a gut microbial enzyme that reduces bilirubin to urobilinogen", Nature Microbiology, vol. 9, no. 1, pp. 173–184, doi:10.1038/s41564-023-01549-x, ISSN   2058-5276 , retrieved 2025-11-18{{citation}}: CS1 maint: multiple names: authors list (link)
  7. ↑ Klaus-Heinrich Röhm (2014), "Pathobiochemie des Aminosäurestoffwechsels", Springer-Lehrbuch, Berlin, Heidelberg: Springer Berlin Heidelberg, pp. 352–356, doi:10.1007/978-3-642-17972-3_28, ISBN   978-3-642-17971-6
  8. ↑ "Gallesekretion und Cholestase - DGIM Innere Medizin". springermedizin.de (in German). Retrieved 2025-11-18.
  9. ↑ Avoxa-Mediengruppe Deutscher Apotheker GmbH. "Bilirubin: Gallenfarbstoff als Krankheitsmarker" (in German). Retrieved 2025-11-18.
  10. ↑ BioRapid GmbH. (2022). Produktinformation Ehrlich’s Reagenz. Abgerufen von https://biorapid.de (Zugriffsdatum: November 2025).
  11. ↑ "Massenspektrometrie (LC-MS/MS)" . Retrieved 2025-11-18.
  12. ↑ Katarina Fischer (2024-01-09). "Warum ist Urin gelb?". National Geographic (in German). Retrieved 2025-11-18.
  13. ↑ Bolsega, S. (2018). Einfluss von intestinaler Mikrobiota auf chronisch-entzündliche Darmerkrankungen im Interleukin-10 defizienten Mausmodell (Unveröffentlichte Dissertation). Tierärztliche Hochschule Hannover.
  14. ↑ Zhang, X. et al. (2023). Gut microbiota dysbiosis in metabolic diseases: From mechanism to therapy. Nature Reviews Endocrinology, 19, 567–584.
  15. ↑ Christoph Küper, Franz-Xaver Beck, Wolfgang Neuhofer (2012-01-01), "Toll-like receptor 4 activates NF-κB and MAP kinase pathways to regulate expression of proinflammatory COX-2 in renal medullary collecting duct cells", American Journal of Physiology-Renal Physiology, vol. 302, no. 1, pp. F38 –F46, doi:10.1152/ajprenal.00590.2010, ISSN   1931-857X {{citation}}: CS1 maint: multiple names: authors list (link)
  16. ↑ Klichi, M. et al. (2024). Leberdiagnostik – Klinische Chemie und Laboratoriumsdiagnostik. In: Vorlesungsskript. Universität Münster.
  17. ↑ Watanabe, M. et al. (2023): Quantitative HPLC-MS analysis of fecal bilinogens as diagnostic markers of liver and microbiome function. Biochemical Pharmacology, 208:115361.
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