Fig. 5: Aspirin improves metabolic outcome in obesogenic conditions in autophagy-dependent manner.

a, b Respectively, WT and Atg4b^−/− male mice, at 10/12 weeks of aspirin treatment were subject to body composition analysis, determined by magnetic resonance imaging (WT mice: n = 10 mice/group; Atg4b^−/− mice: Ctrl = 4 and aspirin = 5 mice). c–j Histological analysis of visceral white adipose tissue (c, d, g, h), liver histopathology (e, f, i, j) were performed and quantified in WT mice (visceral white adipose tissue analysis: Ctrl = 9 and aspirin = 10 mice; liver histopathology: n = 8 mice/group) and Atg4b^−/− mice (visceral white adipose tissue analysis and liver histopathology: Ctrl = 4 and aspirin = 5 mice). Representative images are shown in (d, e, g, i) and quantifications are reported in (d, f, h, j) respectively. In this figure, results are displayed as box and whisker plots, which show median, first and third quartiles, and maximum and minimum values (a, b, f, J) or means ± s.e.m. d, h Circles, in the graphs, indicate each mouse used in the experiment. For statistical analysis, p values were calculated by two-tailed unpaired Student’s t test (a, b, f, j) comparing aspirin-treated to untreated mice (**p < 0.01). Statistical comparisons in (d, h) were done by means of a Kolmogorov–Smirnov test comparing aspirin-treated to control group (***p < 0.001). Atg4b autophagy-related protein 4 homolog B, HFD high-fat diet, WAT white adipose tissues.