Figure 5: Rescue of PPARγ expression in liver causes hypertrophy.
From: PPARγ contributes to PKM2 and HK2 expression in fatty liver
(a) Macroscopic view of WT and AlbCre;PTENf/f;Akt2−/− mice 7 days after adenoviral transduction of GFP or PPARγ. (b) Relative transcript levels and (c) immunoblot analysis of protein levels in livers of mice transduced with GFP or PPARγ adenoviruses for 7 days. Data are means±s.e.m., n=3–5 (P<0.05 (a) versus GFP; 2-tailed, unpaired Student's t test). (d) Liver to body weight ratio of WT mice transduced with adenoviruses expressing GFP or PPARγ and treated with 3BrPA. Data are means±s.e.m., n=5–11 (P<0.05 (a) versus WT; (b) versus PPARγ control; 2-tailed, unpaired Student's t test). (e) Hepatocyte proliferation after PPARγ overexpression is inhibited by 3BrPA treatment. Number of BrdU+ nuclei and total number of hepatocyte nuclei were scored in the livers of mice transduced with indicated adenoviruses treated for 1 day before sacrifice with BrdU in drinking water. Data are presented as a ratio of BrdU+ to total number of nuclei ±s.e.m., n=3–7 (P<0.05 (a) versus GFP; (b) versus PPARγ control; 2-tailed, unpaired Student's t test). (f) Triglyceride concentration in liver tissue of mice transduced with GFP or PPARγ adenoviruses, and treated with 3BrPA. Data are means±s.e.m., n=5–11 (P<0.05 (a) versus GFP; (b) versus PPARγ control; 2-tailed, unpaired Student's t test). (g) H&E staining and immunohistochemistry using anti-PKM2 antibody of liver sections of AlbCre;PTENf/f;Akt2−/− mice 14 days after adenoviral transduction with GFP or PPARγ. Bar represents 100 μm. (h) RT–QPCR analysis of relative transcript levels of glycolytic enzymes in primary WT hepatocytes 40 h postinfection with 5 MOI of adenoviruses expressing GFP or PPARγ. Data are means±s.e.m., n=3 (P<0.05 (a) versus GFP; 2-tailed, unpaired Student's t test). (i) Immunoblot analysis of protein levels of glycolytic enzymes in primary hepatocytes transduced with different doses of PPARγ or GFP adenovirus collected 40 h postinfection. (j) Proposed model of PPARγ contribution to metabolic changes and pathophysiological growth in PTEN-null livers.
