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. 2016 Mar 14;6:23043. doi: 10.1038/srep23043

Figure 3. Oral GlcNAc alters liver metabolism.

Figure 3

(A) Liver free fatty-acids (FFA) and (B) triglycerides (TG) in wild-type C57BL/6 male mice on 4% or 9% fat diet over 30 weeks on oral GlcNAc at 0.5 mg/ml. Data shown are mean ± SEM, n = 5, *p < 0.05, **p < 0.01 and ***p < 0.001 GlcNAc-treated versus control in fasted or fed state with 2-tailed, unpaired Student’s t-test. Immunoblot analysis of metabolic signaling pathways, with fatty-acid synthase (FASN) and phosphorylated forms of Akt kinase, ribosomal protein S6 (S6), AMP-Activated Protein Kinase (AMPK-α) and Acetyl-CoA Carboxylates Kinase (ACC) in liver lysates from mice maintained on 9% fat diet and supplemented with GlcNAc for 30 weeks in ad libitum fed (C) or 18 h fasted (D) states. (E) Intraperitoneal glucagon tolerance test and (F) intraperitoneal glucose tolerance test, with area under the curve (AUC) quantification in mice supplemented with 0.5 mg/ml oral GlcNAc for 23 weeks. Data shown are mean ± SEM, n = 5, *p < 0.05.