Fig. 6: Genetically depleting APCs improves obesity-related metabolic impairments.
Eight-weeks old PD mice were fed with HFD for 3 months and APCs were depleted to investigate the metabolic alterations. Meanwhile, about 3.5×104 CD9- APCs isolated from untreated obese PD mice were transplanted into the eWAT of APC-depleted mice. a Schematic representation of the intervention strategy. TMX, tamoxifen. b After one month, fasting blood glucose levels were measured (chow, n = 6; all other groups, n = 7). Glucose tolerance test (c), insulin tolerance test (d), and pyruvate tolerance test (e) in mice after 1 month of tamoxifen administration (n = 5 per group). Serum and eWAT of all mice were then collected to conduct the following experiments (f–n). Serum levels of FFA (f) and glycerol (g) (chow, n = 6; all other groups, n = 7). The eWAT of mice was cultured in vitro and levels of glycerol (h) and FFA (i) in culture medium were detected at the indicated time points (n = 5 per group). j mRNA level of the indicated genes was determined by qRT-PCR (n = 5 per group). k Representative images showing the staining of APCs in mouse eWAT of four group. White arrows indicate typical stained cells. l–n Frequencies of APC subpopulations in mouse eWAT of four group were detected by flow cytometry (l) and quantified (m,n) (n = 5 per group). Data are means ± SD. For statistical analysis, b–j, m, n One-way ANOVA was used followed by Tukey’s multiple comparison test. Source data are provided as a Source data file.
