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. Author manuscript; available in PMC: 2009 Oct 20.
Published in final edited form as: J Lipid Res. 2006 Jun 21;47(9):2028–2041. doi: 10.1194/jlr.M600177-JLR200

Fig. 5.

Fig. 5

Effect of glucose on elongase and desaturase expression. A: Primary rat hepatocytes in Williams E medium + 10 mM lactate + dexamethasone + insulin were switched to Williams E medium + 25 mM glucose + dexamethasone + insulin. After 24 h of treatment, cells were harvested for extraction of nuclear proteins and RNA. The nuclear abundance of carbohydrate-regulatory element binding protein (ChREBP) and MAX-like factor X (MLX) was measured by immunoblotting at the times indicated (22). B: L-type pyruvate kinase (L-PK), Elovl-6, and Δ9D mRNA abundance was quantified by qRT-PCR (transcript/ cyclophilin). Results are expressed as fold induction by glucose (means ± SD; n = 4). C: In a second experiment, primary hepatocytes in Williams E medium + 10 mM lactate + dexamethasone + insulin remained uninfected (white bars) or were infected with recombinant adenovirus expressing luciferase (Ad-Luc; black bars) or dominant negative MLX (Ad-dnMLX; gray bars). After 24 h, cells were switched to Williams E medium + 25 mM glucose + dexamethasone + insulin. Twenty-four hours later, cells were harvested for RNA extraction and measurement of L-PK, Elovl-6, and Δ9D mRNA by qRT-PCR (transcript/cyclophilin). Results are represented as relative mRNA abundance relative to glucose-treated cells (means ± SD; n = 4). Results are representative of two separate studies. * P < 0.001 versus glucose-treated cells by ANOVA.