Fig. 1. Effects of liver GS deficiency on glutamine metabolism.
a, GS-catalyzed reaction. b, Administration of AAV8-TBG-Cre in mice with wt/wt, Glulwt/tm3Whla fl and Glultm3Whla fl/tm3Whla fl genotypes results in mice with wt/wt, wt/Δ and Δ/Δ livers, respectively. c, Serial sections of mouse liver stained by IHC for GS and OAT, two markers of pericentral zones; scale bar, 1 mm. The insets show magnifications of the central vein (c) and portal vein (p); scale bar, 100 µm. The images shown are representative of three mice per genotype. d, Immunoblot of liver samples obtained from n = 3 mice per genotype. β-Actin is shown as a loading control. e,f, Glutamine levels in wt/wt (n = 9), wt/Δ (n = 9) and Δ/Δ (n = 12) livers (e) and sera (f) measured by LC–MS. g,h, Glutamate levels in the livers (g) and sera (h) of wt/wt (n = 9), wt/Δ (n = 9) and Δ/Δ (n = 12) mice. i, Ammonia concentration in blood samples from wt/wt (n = 11) and Δ/Δ (n = 12) mice. j,k, Glutamine (j) and glutamate (k) levels in the blood collected from mice 4 h after administration of vehicle (n = 4) and MSO (n = 4). l, Glutamine levels in the liver, brain, muscle and pancreas from mice treated as in j (n = 4 vehicle, n = 4 MSO). Data in e–l were analyzed by two-tailed Student’s t-test. Bars represent mean ± s.e.m., and each circle represents data from a single mouse.