However, as lipid consumption through FA oxidation is decreased by MIR20B , free OA or oleyl-CoA might be maintained at a stably increased level compared to that of OA-untreated MIR NC or MIR20B condition, and the impact of the changes in OA or oleyl-CoA levels on the transcriptional phenotype might not be significant as found in a constant elevated level of MIR20B by OA.
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Hepatic <i>MIR20B</i> promotes nonalcoholic fatty liver disease by suppressing <i>PPARA</i>.
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