Fig. 1: Hyperammonemia enhances hepatic O-GlcNAcylation.
From: O-GlcNAcylation enhances CPS1 catalytic efficiency for ammonia and promotes ureagenesis
a Schematic depiction of the HBP and O-GlcNAcylation. Glutamine and uridine feed into the HBP that produces UDP-GlcNAc, while GFPT1 is the rate-limiting step of UDP-GlcNAc synthesis. Protein O-GlcNAcylation is operated by OGT while OGA removes the O-GlcNAc from proteins. b Hepatic content of glutamine, uridine and UDP-GlcNAc in livers of C57BL/6 wild-type (WT) mice at 1.0 h after the intraperitoneal (i.p.) injection of ammonium chloride (NH4Cl) (10 mmol/kg) compared to livers of mice that received i.p. injection of sodium chloride (Control) (n = 5 mice/group). p = 0.0234, p = 0.0219, p = 0.0225. (Unpaired t-test). c, d Western blots and densitometric quantifications of GFPT1, OGT and OGA in livers of WT mice harvested 1.0 h after the i.p. injection of either sodium chloride (Control) or NH4Cl (10 mmol/kg) (n = 5 mice/group). e Western blot for O-GlcNAc proteins with RL2 antibody in livers of WT mice harvested at 0.5 and 1.0 h after i.p. injections of NH4Cl (10 mmol/kg) compared to sodium chloride-injected mice. Samples were run on the same gel but were non-contiguous. f Representative immunohistochemistry images for O-GlcNAc proteins in livers of WT mice harvested 0.5 h after the i.p. injection of either sodium chloride (Control) or NH4Cl (10 mmol/kg). Scale bars: 100 μm. GAPDH was used as loading control. All values are shown as averages ± SEM. ns, no statistically significant difference. Experiments in panels e and f were performed twice.
