An in vitro model to study the adipose tissue toll-like receptor -mediated effects of gut microbiota on non-alcoholic fatty liver disease development
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2017Alkoholista riippumaton rasvamaksa (NAFLD) on maailman yleisin maksasairaus ja saattaa johtaa kirroosin tai maksasyövän kehittymiseen. Viimeaikaisissa tutkimuksissa suolistosta peräisin olevin bakteerimolekyylien, kuten flagelliinin (FLG) ja lipopolysakkaridien (LPS), rooli rasvamaksan kehittymisessä on tunnistettu. Nämä molekyylit saattavat vaikuttaa maksaan välillisesti rasvakudoksen kautta toll-like reseptorien (TLR) signaalireittejä aktivoiden. Tässä tutkimuksessa selvitettiin FLG:n ja LPS:n rasvasoluvälitteisiä vaikutuksia HepG2-hepatoomasoluihin. Hypoteesina oli, että FLG ja LPS lisäisivät HepG2 soluissa rasvan kerääntymistä, insuliiniresistenssiä ja tulehdusta, joita mitattiin kvantitatiivisella PCR:llä sekä western blotilla. Tulokset osoittavat, että FLG saattaa vaikuttaa rasvamaksan kehitykseen erityisesti adiposyyttien kautta. Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the world, and may lead to development of cirrhosis or hepatocellular carcinoma. Lately the role of molecules from gut-derived bacteria, like flagellin (FLG) and lipopolysaccharides (LPS) in development of NAFLD has been recognized. These molecules could affect the liver indirectly through activation of adipose tissue toll-like receptor (TLR) pathways. In this study the potential adipocyte mediated effects of FLG and LPS on HepG2 hepatoma cells were explored. The hypothesis was that FLG and LPS would increase HepG2 fat accumulation, insulin resistance and inflammation measured with quantitative realtime PCR (qPCR) and western blot. According to the results especially adipocyte mediated FLG could have a role in fatty liver development.
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