To understand the molecular basis of lipid reduction in liver, we measured expression of SREBP1, SREBP2, ChREBP and FAS.
To assess oxidative injury in the liver, we measured the hepatic TBARS levels.
To examine the efficiency of gankyrin overexpression in the liver, we measured gankyrin expression in four different transgenic lines with RT-PCR and western blot assay.
To investigate whether ATGL-ko mice exhibit reduced neutral REH activity in liver, we measured REH activity in lipid-poor lysates (20.000 × g infranatant) prepared from total liver, from isolated hepatocytes, or from isolated non-parenchymal cells (NPCs).
Because ST-1 treatment significantly decreased the CYP1A1 and CYP1A2 mRNA levels only in wild-type mouse liver, we measured the expressions of AhR mRNA and protein in wild-type mouse liver.
To determine if PNPLA3-148M accumulatesecondaryry to the development of fatty liver, we measured PNPLA3 mRNA and protein in livers from mice fed a high-fat diet for 12 weeks (Supporting Fig. 6A).
To study whether administration of a vitamin A-deficient diet for 15 weeks led to the vitamin A deficiency in the plasma and liver, we measured retinol concentrations by HPLC in these tissues.
To explore the source of LPL released into plasma and taken up by the liver we measured LPL activity in adipose tissue and heart before and after injection of heparin.
In isolated mitochondria from mouse liver, we measured the effects of PGZ treatment on MRC complex activities, fully-assembled complex I and its subunits, gene expression of complex I and III subunits, and [H]PGZ binding to mitochondrial complexes.
To explore the origin of the LPL released into plasma and taken up by the liver we measured LPL activity in heart and adipose tissue before and 20 min after injection of heparin (Table 2).
