Figure 6: Hepatic AA/mTORC1/S6K activation raises serum TGs via a neuronal relay.

Rheb (black bars) (a–g) or SNAT2 (black bars) (h–j) and control LacZ (white bars), adenoviruses were administered. (a and b) Vehicle (Veh) or bupranolol (Bup) was intraperitoneally administered to standard chow-fed C57BL/6 mice 5 days after adenoviral administration. Serum TG levels and HPLC results of sera in fed states were measured (a), and LPL mRNA expression in WAT was examined (b) 60 min after this administration (a; n=4–6, b; n=6–7). (c–e) Standard chow-fed C57BL/6 mice were subjected to sham operation (Sham) or HV 7 days before adenoviral administration. Serum TG levels in fed states were measured (c), sera in fed states were analysed by HPLC (d) and LPL mRNA expressions in WAT were determined (e) on day 5 after adenovirus administration (c; n=6–7, d; n=4–5, e; n=6–7). (f,g) Vehicle (Veh) or capsaicin (Cap) was applied to the hepatic vagus of standard chow-fed C57BL/6 mice 7 days before adenoviral administration. Serum TG levels in the fed state were measured (f) and LPL mRNA expression in WAT was examined (g) on day 5 after adenovirus administration (f; n=6–8, g; n=6–7). (h–j) The C57BL/6 mice were subjected to sham operation (Sham) or HV 7 days before adenoviral administration. Serum TG levels in fed states were measured (h and i), and the ratios of LPL mRNA expression in WAT, as compared with controls, were examined (j) on day 5 after adenovirus administration (h; n=4–5, i; n=4–5, j; n=5). Data are presented as means±s.d. *P<0.05, **P<0.01 by the unpaired t-test. NS, not significant.