Figure 4: Pharmacological activation of PPARγ by Pioglitazone promotes growth of PTEN-null liver.
From: PPARγ contributes to PKM2 and HK2 expression in fatty liver
(a) Blood glucose level of random-fed mice of the indicated genotypes. Data are means±s.e.m., n=8 (P<0.05 (a) versus WT; (b) versus control; 2-tailed, unpaired Student's t test). (b) Liver- to body-weight ratio of WT and AlbCre;PTENf/f mice after PIO treatment. Data are means±s.e.m., n=5–8 (P<0.05 (a) versus WT; (b) versus control; 2-tailed, unpaired Student's t test). (c) Increased proliferation rate of hepatocytes after PIO treatment. Number of BrdU+ nuclei and total number of hepatocytes nuclei were scored in the liver of untreated and PIO-treated mice, 5 days after administration of BrdU in drinking water. Data presented as a ratio of BrdU+ to total number of nuclei ±s.e.m., n=4–8 (P<0.05 (a) versus WT; (b) versus control, 2-tailed, unpaired Student's t test). (d) Immunoblot analysis of liver extracts of WT and AlbCre;PTENf/f mice treated with or without PIO.
