Extended Data Fig. 5: Adipocyte-specific deletion of Paqr4 improves glucose homoeostasis in obesity.
From: PAQR4 regulates adipocyte function and systemic metabolic health by mediating ceramide levels
(a-b) Specific recombination of Paqr4 (representative images from 3 independent assays with similar results) and downregulation in gene expression levels in Paqr4iAKO mice fed dox chow for 2 weeks (n = 6). (c-d) Comparable body weight and body composition in Paqr4iAKO mice fed dox chow for 20 weeks (Paqr4fl/fl, n = 7; Paqr4iAKO, n = 6). (e) Tissue weights in Paqr4iAKO mice fed dox chow for 20 weeks (n = 6). (f-g) Comparable glucose tolerance and insulin sensitivity after 8-9 weeks of dox chow feeding (Paqr4fl/fl, n = 7; Paqr4iAKO, n = 6). (h-j) Moderately improved glucose tolerance and insulin-mediated glucose disposal after 19-20 weeks of dox chow feeding (Paqr4fl/fl, n = 7; Paqr4iAKO, n = 6). (k-p) Comparable food intake, RER, VO2, VCO2, energy expenditure (EE), and physical activity after 15 weeks of dox-HFD feeding (n = 6). (q-r) Body composition and tissue weights after 20 weeks of dox-HFD feeding (Paqr4fl/fl, n = 16; Paqr4iAKO, n = 22). (s-u) Slightly improved glucose tolerance in Paqr4iAKO mice after 2 and 8 weeks and insulin-mediated glucose disposal after 9 weeks of dox-HFD feeding (Paqr4fl/fl, n = 16; Paqr4iAKO, n = 22). Data shown as mean ± SEM and analysed by two-tailed unpaired t-test (b, d-e, l-r) and two-way ANOVA (c, f-k, s-u).
