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. 2019 Jun 17;294(31):11944–11951. doi: 10.1074/jbc.RA119.008778

Figure 2.

Figure 2.

IMP2 inactivation diminishes palmitate oxidation by hepatocytes and liver mitochondria and binds mRNAs encoding mediators of fatty acid oxidation. A, [1-C14]palmitate oxidation by hepatocytes from Imp2ff and Imp2ff/Alb-Cre+/− mice. Hepatocytes were isolated from six pairs of Imp2ff and Imp2ff/Alb-Cre+/− male mice 6 weeks of age, 2 weeks on the HFD, and assayed in triplicate for their ability to oxidize [1-C14]palmitate with or without etoximir (0.1 mm). Mean values are indicated in red. ns, p > 0.05. B, [1-C14]palmitate oxidation by mitochondrial fractions from Imp2ff and Imp2ff/Alb-Cre+/− livers. Mitochondria were isolated from the livers of nine pairs of Imp2ff and Imp2ff/Alb-Cre+/− male mice 6 weeks age, 2 weeks on the HFD, and assayed in triplicate for their ability to oxidize [1-C14]palmitate. C, liver RNAs enriched in an IMP2 IP. Extracts from the livers of three pairs of 30-week-old HFD-fed male Imp2ff and 8 Imp2ff/Alb-Cre+/− mice were incubated with anti-IMP2 or nonimmune IgG. RNA was extracted from the washed IPs, and the indicated mRNAs were quantified by QPCR. The ratio of mRNA abundance in IMP2 IP/nonimmune IP is shown. *, p < 0.05; **, p < 0.01.