Fig. 2: Myeloid GPSM1 abrogation protects mice from diet-induced obesity and metabolic dysfunction.

Male GPSM1^f/f; Lyz2-cre mice and age-matched GPSM1^f/f littermates were fed a HFD for 12 weeks. HFD feeding started at 7 weeks of age. a Body weight (n = 12 biologically independent for GPSM1^f/f and n = 10 biologically independent for GPSM1^f/f; Lyz2-cre mice). b Percent of fat (left) and lean (right) body mass (n = 9 biologically independent mice per group). c fat-pad weights (n = 9 biologically independent mice per group). d Hematoxylin and eosin (H&E) staining of eWAT and scWAT sections. Scale bars, 100 μm. Independent experiments were repeated three times with similar results. e Serum concentration of adiponectin and leptin (n = 8 biologically independent mice per group). f Serum insulin levels (n = 8 biologically independent mice per group). g Fasting glucose levels (n = 8 biologically independent mice per group). h Glucose tolerance test and AOC (area over the curve), n = 9 biologically independent mice per group. i Insulin tolerance test and AOC (area over the curve), n = 10 biologically independent mice per group. j Immunoblots of AKT phosphorylation in murine eWAT, liver and muscle after insulin administration (1.5 U/kg) or PBS in vivo. k Representative images of H&E staining (top) and Oil Red O (bottom) staining of liver sections and quantification (n = 5 biologically independent mice per group). Scale bars, 100 μm. l Liver weight (n = 9 biologically independent mice per group). m Quantification of hepatic triglycerides (n = 8 biologically independent mice per group). n Serum levels of total cholesterol (TCH), non-esterified fatty acid (NEFA), ALT, and AST (n = 9 biologically independent mice per group). All data are shown as means ± SEM. P values are determined by two-way analysis of variance (ANOVA) with Sidak’s multiple-comparisons test (a, h, and i) or unpaired two-tailed Student’s t-test (b, c, e to i, and k–n).