
A new study has employed human fetal hepatocyte organoids to model the early stages of nonalcoholic fatty liver disease (NAFLD). The researchers used organoids to model several drivers of steatosis, including genetic risk factors and monogenic lipid disorders. Target discovery and drug screening identified steatosis-resolving compounds. In addition, the researchers developed a CRISPR-based screening platform (termed FatTracer) to identify modulators or targets of steatosis, specifically using organoid models of monogenic lipid disorders (APOB−/− and MTTP−/−). The study identified fatty acid desaturase 2 (FADS2) as a key modulator of hepatic steatosis.
Like
Save
Share