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. 2011 Sep 9;286(44):38128–38135. doi: 10.1074/jbc.M111.256677

FIGURE 2.

FIGURE 2.

LCN13 promotes fatty acid β-oxidation in primary hepatocytes. A, primary hepatocytes were infected with β-gal or LCN13 adenoviruses, and fatty acid β-oxidation rates were measured 16 h after viral infection. B, primary hepatocytes were treated with the conditioned medium for 16 h and subjected to β-oxidation assays. C, primary hepatocytes were treated with recombinant LCN13 protein for 16 h and subjected to β-oxidation assays. D, primary hepatocytes were stimulated with LCN13 in the absence (Basal) and presence of glucagon (50 nm). Ketone body secretion was measured 8 h after stimulation. E, primary hepatocytes were infected with β-gal or LCN13 adenoviruses. Total RNAs were extracted 16 h after infection and used to measure mRNA abundance by qRT-PCR. The expression of individual genes was normalized to 36B4 expression. Error bars represent S.E. *, p < 0.05. a.u., arbitrary units; MCAD, medium-chain acyl-CoA dehydrogenase; LCAD, long-chain acyl-CoA dehydrogenase.