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. 2009 Feb 10;106(9):3354–3359. doi: 10.1073/pnas.0802864106

Fig. 5.

Fig. 5.

Pancreatic exocrine insufficiency induces mitochondrial β-oxidation. (A) Expression analysis of genes involved in fatty acid uptake and β-oxidation in the (A) pancreas, (B) liver, (C) muscle, and (D) fat tissue of p48-Kras mice and Kras control littermates on a HFD were measured by Real-Time PCR. (E) TEM pictures showing pronounced ultrastructural changes (arrowhead with a star) in hepatic mitochondria (arrowhead) in p48-Kras mice and Kras control littermates on the HFD. N, nucleus; L, lipid droplet. (F) Liver transaminases, ALT and AST, were analyzed in p48-Kras mice and Kras control littermates on the HFD. (G–J) Expression analysis of genes involved in lipid metabolism in (G) pancreas, (H) liver, (I) muscle, and (J) fat tissue of TNFR1−/−-p48-Kras mice and TNFR1−/−-Kras control littermates on the HFD were measured by Real-Time PCR. (K) TEM pictures showing ultrastructure of hepatic mitochondria (arrowhead) in TNFR1−/−-p48-Kras mice on HFD. N, nucleus; L, lipid droplet. (L) Schematic drawing suggesting how the HFD enhances pancreatic tumorigenesis. Data are mean values ± SEM. N = 4–7 mice per genotype. *, P ≤ 0.05.