Fig. 4

Clec7a-deficient mice are resistance to diet-induced obesity. A Intestinal gene expressions of Clec2d, Clec4a, and Clec7a in lean and obese mice fed HFD via RT-PCR (n = 8). B Intestinal gene expressions of Clec2d, Clec4a, and Clec7a in HFD-fed mice via RT-PCR (n = 7–11). C–H Body weight (C), the relative weight of white adipose tissues (D), serum TC (E), serum TG (F), and adipocyte area (HE staining, × 400) of SAT (G) and PEAT (H) in HFD mice treated with curdlan (Cur). C57BL/6 mice (7 weeks old, male) fed HFD or curdlan (10 mg/mouse) for 18 weeks to test the role of Clec7a activation in obesity (n = 8–16). I–K Final body weight (I), the relative weight of SAT (J), and epididymal adipose tissue (EAT) (K) in Clec7a KO mice. Seven-week-old-male C57BL/6 wild-type and Clec7a KO mice were fed HFD for 14 weeks (n = 7 or 11). L–N Metabolic parameters (O₂, CO₂, and energy consumption) of Clec7a KO mice (n = 6). O Lipid metabolic genes of SAT in Clec7a KO mice (n = 7 or 11). Differences among the groups were compared using Student’s t-test. *p < 0.05; **p < 0.01; ***p < 0.001; ns p > 0.05