Fig. 3: Cd36ΔLEC mice develop spontaneous obesity and adipose tissue inflammation.
From: Visceral obesity and insulin resistance associate with CD36 deletion in lymphatic endothelial cells
a Body weight (g) of female and male 20-week LEC Cd36 deficient (Cd36ΔLEC) mice is increased as compared with sex-matched control mice (n = 8); female, P = 0.016; male, P < 0.01. b Body composition analysis shows similar lean mass between age- and sex-matched controls and Cd36ΔLEC mice (female, P = 0.327; male, P = 0.154), whereas fat mass is higher in both female and male Cd36ΔLEC mice (both P < 0.01) as compared with sex-matched controls (n = 8). c Representative images of visceral (epididymal and mesenteric) and subcutaneous fat pads from male mice. d Weight (g) of epididymal (Epi) and subcutaneous (Subcut) fat pads is increased (all P < 0.01) in Cd36ΔLEC mice as compared with controls (n = 5). e, f Levels of plasma glucose and area under the curve (AUC) during an oral glucose tolerance test in 11- and 20-week-old mice (n = 5). Glucose disposal is impaired in Cd36ΔLEC mice at 20 weeks as compared with age-matched controls (P < 0.01). g Gene expression analysis in epididymal adipose tissue in 11- and 20-week-old Cd36ΔLEC and age-matched control mice (n = 5). As compared with age-matched controls, 11-week-old Cd36ΔLEC mice show increased gene expression of tumor necrosis factor alpha (Tnf, P < 0.01) and of EGF module-containing mucin-like receptor 1 (Emr1, P < 0.05). The 20-week-old Cd36ΔLEC mice show increased gene expression of lipoprotein lipase (LpL, P < 0.001), peroxisome proliferator-activated receptor gamma (Pparg, P < 0.001), Tnf (P < 0.001) interleukin-6 (Il6, P < 0.001), tumor growth factor-beta (Tgfb1, P < 0.001) and Emr1 (P < 0.001). A.U. arbitrary units. All data are means ± SE with n representing the number of mice per group. Statistical significance is determined by two-tailed Student t test. *P < 0.05; **P < 0.01, ***P < 0.001.
