Fig. 7: FGF21-mediated reversal of defective autophagy and hepatosteatosis in obese mice is dependent on JMJD3. | Nature Communications

Fig. 7: FGF21-mediated reversal of defective autophagy and hepatosteatosis in obese mice is dependent on JMJD3.

From: Fasting-induced FGF21 signaling activates hepatic autophagy and lipid degradation via JMJD3 histone demethylase

Fig. 7

JMJD3-floxed mice fed a HFD for 4 weeks were injected with the indicated viruses and then treated with vehicle or FGF21 every 2 days for 4 weeks with continued feeding of a HFD. a–f n = 5 mice/group, g n = 3 mice/group. a Experimental outline (top), body weights, food intakes, and images of liver. b Neutral lipids in liver sections stained with H&E and Oil Red O detected by IHC (left) and liver TG levels (right) (scale bar = 50 μm). c Levels of liver acylcarnitine species (left) and serum β-hydroxybutyric acid (β-HDB) (right). d Glucose tolerance test (GTT). e O2 consumption (left) and CO2 production (right) rates measured by indirect calorimetry. f Relative mRNA levels of the indicated hepatic proteins. g Levels of the indicated proteins in liver extracts from mice measured by IB with the LC3-II/I ratio and p62 band intensities shown below the blot (left), liver sections with LC3 detected by IHC (middle), and the number of LC3-II puncta/cell (right, n = 10 hepatocytes) (scale bar = 10 μm). Source data are provided as a Source Data file. a–g Values are presented as mean ± SD. Statistical significance was measured using the (b, c, e line graph, f, g) one-way or d two-way ANOVA with the Bonferroni post-test, and (e, bar graph) Student’s t-test. *P < 0.05, **P < 0.01, and NS statistically not significant.

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