Fig. 5. Fungal lipases from C. parapsilosis contribute to the HFD-induced obesity in mice.

The HFD-fed mice were pretreated by addition of amphotericin B in the drinking water for two weeks, and then orally given with the live C. parapsilosis (CP^WT) or the live lipase-negative mutant strain of C. parapsilosis (CP^KO) for 7 weeks. a Experimental design; b weight gain; c macroscopic views of mice; d representative H&E staining of the adipose tissue; e plasmatic cholesterol; f plasmatic TG; g plasmatic free fatty acid; h hepatic total cholesterol, LDL-C, and HDL-C; i hepatic triglyceride; j plasma aspartate transaminase (AST) and plasma alanine transaminase (ALT); k representative H&E staining and Oil Red O staining of the liver; l fecal lipase activity; m fecal FFAs level; n relative mRNA expression of CD36 among the intestinal tract. HFD, high-fat diet-fed mice group; HFD + Ampho, high-fat diet-fed mice treated with amphotericin B; HFD + CP^WT, high-fat diet-fed and fungi-free mice treated with live C. parapsilosis; HFD + CP^KO, high-fat diet-fed and fungi-free mice treated with live lipase-negative mutant strain of C. parapsilosis. Data are presented as the mean ± SEM. b, e−j and l, m N = 8−10 mice per group, n N = 6 mice per group. Statistical analysis was performed using one-way ANOVA followed by the Tukey post hoc test for (e−j), (l−n), and two-way ANOVA followed by the Bonferroni post hoc test for (b). *p < 0.05; **p < 0.01; ***p < 0.001.