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. 2008 Jul;49(7):1538–1552. doi: 10.1194/jlr.M800123-JLR200

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Copyright © 2008, American Society for Biochemistry and Molecular Biology, Inc.

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Fig. 2. — Overexpressed Elovl-2 and Elovl-5, but not Elovl-6, attenuate fatty acid induction of peroxisome proliferator-activated receptor α (PPARα)-regulated genes in rat primary hepatocytes. Rat primary hepatocytes were either not infected or infected with recombinant adenovirus expressing acyl-CoA synthetase-4 (ACS-4; A), Elovl-2 (A, B), Elovl-5 (B), or Elovl-6 (B) (see Materials and Methods). Cells were incubated in Williams E containing 25 mM glucose, 50 μM BSA, 10 nM dexamethasone, and 1.0 μM insulin in the absence or presence of 250 μM 20:5,n-3 for 24 h. After fatty acid treatment, RNA was extracted and assayed for mRNA abundance of cytochrome P450 4A (CYP4A), mitochondrial hydroxymethylglutaryl-CoA synthase (mtHMG-CoA synthase), sterol-regulatory element binding protein-1 (SREBP-1), and L-type (liver) pyruvate kinase (L-PK; A) by Northern analysis (34) or of cytosolic fatty acid thioesterase-1 (CTE1; B) by quantitative real-time PCR (Table 1; see Materials and Methods) (17). Results are expressed as fold change in mRNA induced by 20:5,n-3 treatment (mean ± SD, n = 6). * P ⩽ 0.05, no infection versus Ad-Elovl2 or Ad-Elovl5.

Fig. 2. — Overexpressed Elovl-2 and Elovl-5, but not Elovl-6, attenuate fatty acid induction of peroxisome proliferator-activated receptor α (PPARα)-regulated genes in rat primary hepatocytes. Rat primary hepatocytes were either not infected or infected with recombinant adenovirus expressing acyl-CoA synthetase-4 (ACS-4; A), Elovl-2 (A, B), Elovl-5 (B), or Elovl-6 (B) (see Materials and Methods). Cells were incubated in Williams E containing 25 mM glucose, 50 μM BSA, 10 nM dexamethasone, and 1.0 μM insulin in the absence or presence of 250 μM 20:5,n-3 for 24 h. After fatty acid treatment, RNA was extracted and assayed for mRNA abundance of cytochrome P450 4A (CYP4A), mitochondrial hydroxymethylglutaryl-CoA synthase (mtHMG-CoA synthase), sterol-regulatory element binding protein-1 (SREBP-1), and L-type (liver) pyruvate kinase (L-PK; A) by Northern analysis (34) or of cytosolic fatty acid thioesterase-1 (CTE1; B) by quantitative real-time PCR (Table 1; see Materials and Methods) (17). Results are expressed as fold change in mRNA induced by 20:5,n-3 treatment (mean ± SD, n = 6). * P ⩽ 0.05, no infection versus Ad-Elovl2 or Ad-Elovl5.