title: High-dose biotin may down-regulate hepatic expression of acute phase reactants by mimicking the physiological role of nitric oxide.
abstract: There is recent evidence that nitric oxide blocks IL-6 signaling in hepatocytes by inhibiting activation of Stat3. If this effect is mediated by cGMP, then high-dose biotin--which can directly activate guanylyl cyclase--may have the potential to suppress hepatic production of acute phase proteins.
mesh_terms: D000210:Acute-Phase Reaction; D000818:Animals; D001710:Biotin / Q000378:metabolism / Q000494:pharmacology*; D002478:Cells, Cultured; D006152:Cyclic GMP / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D015536:Down-Regulation; D006801:Humans; D007249:Inflammation; D008099:Liver / Q000201:enzymology; D008962:Models, Theoretical; D009569:Nitric Oxide / Q000378:metabolism*; D051381:Rats; D050796:STAT3 Transcription Factor; D015398:Signal Transduction; D015534:Trans-Activators / Q000378:metabolism; D000093242:Interleukin-6 Inhibitors
chemical_list: D001710:Biotin; D006152:Cyclic GMP; D004268:DNA-Binding Proteins; D009569:Nitric Oxide; D050796:STAT3 Transcription Factor; D015534:Trans-Activators; D000093242:Interleukin-6 Inhibitors; C494086:STAT3 protein, human; C494088:Stat3 protein, rat