Fig. 4.

Impaired AT-lipolysis counteracts hepatic stress and TG accumulation via promoting hepatic TG catabolism on high fat diet. (A) Organ weights of mice kept on high fat diet (HFD) for 10 weeks starting at the age of 5 weeks. (B) Hepatic TG and TC content upon HFD-feeding in fasted mice. (C) Representative images of hepatic tissue morphology analyzed by transmission electron microscopy (Scale bar = 1 μm; LD, lipid droplet; m, mitochondria; n, nucleus). (D) TG hydrolytic activities in liver tissue of fasted mice. (E) Hepatic mRNA levels of selected PPARα- and CREBH-regulated genes of fasted flox/flox and CGI-58-ATko mice determined by qRT-PCR. (F) Hepatic G0S2 and (G) nuclear CREBH protein expression on chow compared to HFD in fasted mice normalized to β-actin and Lamin A/C, respectively (n = 3). (H) Ratio of phosphorylated JNK vs. total JNK. (I) PCR-amplification of non-spliced and spliced Xbp1 (171 bp and 145 bp, respectively) from hepatic cDNA separated by agarose gel electrophoresis. (J) Simplified scheme depicting the role of AT-derived FAs in the regulation of fasting gene expression in the liver. Values are mean ± SD from at least 5 mice per genotype. ^*p <0.05, ^**p <0.01, and ^***p <0.001 flox/flox vs. CGI-58-ATko (on chow or HFD). (This figure appears in colour on the web.)