Fig. 5.

Pharmacological activation of Akt by IGF-1 alleviated chronic ethanol-induced fatty liver in mice. Mice were treated with recombinant IGF-1 (100 μg/kg body weight, in IGF/ethanol group) or equal volume of sterile saline (in Control and Ethanol groups), and exposed to ethanol-containing liquid diet or control diet for 4 weeks. Histological examination and the determination of liver TG levels showed that IGF-1 significantly suppressed chronic ethanol-induced fat accumulation in liver sections and the increase of hepatic TG level (a) & (b); Results of western blotting showed that IGF-1 treatment increased the phosphorylation of Akt at ser473 and thr308, and also increased the phosphorylation of GSK3β at ser9 (c). **P<0.01, compared with the Control group mice; ^#P<0.05, ^##P<0.01, compared with the ethanol group mice.