Fig. 2: Deletion of Nogo-A/B improves hepatic glucose metabolism without affecting body weight in lean mice. | Nature Communications

Fig. 2: Deletion of Nogo-A/B improves hepatic glucose metabolism without affecting body weight in lean mice.

From: Suppression of endothelial ceramide de novo biosynthesis by Nogo-B contributes to cardiometabolic diseases

Fig. 2

A Schematic representation of the experimental design. All the analysis in this figure were conducted on male WT and Nogo-A/B-deficient mice SD-fed for 6 months (Created in BioRender. Di Lorenzo, A. (2025) https://BioRender.com/i50g226). B Body weight (n = 18 mice per group), C Fat mass, lean mass and total water content (n = 5 mice per group). D Total, dark phase, and light phase food intake, expressed as average of 3 consecutive days (n = 5 mice per group). E Plasma glucose levels after o.n. starvation (WT SD n = 14 mice and Nogo-A/B-deficient SD n = 9 mice). F GTT (WT SD n = 19 mice and Nogo-A/B-deficient n = 13 mice) and G ITT (n = 9 mice per group). H Plasma insulin levels pre- and post-glucose administration (i.p., 1.5 g/kg). (WT SD n = 8 mice and Nogo-A/B-deficient SD n = 7 mice). I Immunofluorescence staining for glucagon, insulin and NOGO-A/B in pancreatic sections of SD WT mice. Nogo-A/B-deficient pancreas were used as negative controls. J PTT (WT SD n = 15 mice and Nogo-A/B-deficient SD n = 8 mice) and K G6Pase mRNA levels in the liver (n = 5 mice per group). L PTT in WT and Nogo-A/B-deficient mice treated with vehicle or Myriocin (0.3 mg/kg, o.n.) (WT SD vehicle n = 8 mice, WT SD treated with myriocin n = 10, Nogo-A/B-deficient SD vehicle n = 8 mice and Nogo-A/B-deficient SD treated with myriocin n = 10). M Immunohistochemistry for NOGO-A/B in liver of lean mice. Nogo-A/B deficient liver were used as negative control. N Glucose production from hepatocytes isolated from WT mice, treated with vehicle or S1P (1 μM, 6 h), and/or W146 (1 μM, 6 h) (n = 3 independent experiments). O PTT in WT male mice on SD after 30 min from intraperitoneal administration of W146 (3 mg/kg) or vehicle (DMSO:water, 1:1) after o.n. starvation (WT SD vehicle n = 6 mice, WT SD treated with W146 n = 8, Nogo-A/B-deficient SD vehicle n = 5 mice and Nogo-A/B-deficient SD treated with W146 n = 7). Data were expressed as mean ± SEM. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. Statistical analysis was performed with unpaired t-test two-tailed (B–E, K), one-way ANOVA (N) and two-way ANOVA with Sidak multiple comparisons test (F, G, H, J, L, O). Source data are provided as a Source Data file.

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