Figure 3: Activation of hepatic mTORC1/S6K pathway leads to hypertriglyceridemia.

(a–c) Rheb (black bars) or LacZ (white bars) adenovirus was administered to C57BL/6 mice. (a) Immunoblotting of liver extracts with anti-phospho-mTOR, mTOR, phospho-p70-S6K, p70-S6K, phospho-S6 and S6 antibodies. Serum TG levels under 10 h-fasted or -fed conditions were measured (b), HPLC results of sera in fed states were determined (c) on day 5 after adenovirus administration (b; n=5–7, c; n=4). (d) CA-S6K (black bars) or LacZ (white bars) adenovirus was administered to C57BL/6 mice. Serum TG levels under 10 h-fasted or -fed conditions were measured, and HPLC results of sera in fed states were determined on day 5 after adenovirus administration (n=4–6). (e–j) Rheb (black bars) or LacZ (white bars) adenovirus was administered to C57BL/6 mice. (e) Fat-tolerance tests were performed, followed by HPLC analysis (n=4–8). (f) TG-clearance studies were performed (n=5–6). (g) Plasma TG-hydrolysis activity was measured after the injection of heparin into the tail veins of 4 h-fasted mice (n=6–8). (h) LPL mRNA expression in WAT was analysed by RT–PCR (n=6–7). (i) Immunoblotting of WAT extracts with anti-LPL antibody. (j) TG-hydrolysis activity in WAT was examined on day 5 after adenovirus administration (n=6–7). The representative images derived from at least two experiments were displayed (a and i). Data are presented as means±s.d. *P<0.05, **P<0.01 by the unpaired t-test. NS, not significant.