Fig. 1: Clstn3 knockout mice show reduced body mass with improved leptin sensitivity and increased energy expenditure.
From: Neural regulation of energy and bone homeostasis by the synaptic adhesion molecule Calsyntenin-3
a qPCR analysis of Clstn3 in the hypothalamus of normal chow (NCD) or HFD-fed mice (n = 12). b Body weight of mice fed a NCD (n = 7 for wild-type and n = 8 for KO mice). c Body weight of mice fed a HFD from 8 weeks of age (n = 6 for wild-type and n = 4 for KO mice). d Representative H&E staining of epididymal WAT and BAT of 17-week-old mice. Scale bar, 0.1 mm. e Quantification of adipocyte size distribution in WAT (n = 7 for wild-type and n = 8 for KO mice). f Fed or fasted blood glucose levels in 16-week-old male mice (n = 5 for wild-type and n = 7 for KO mice). g Glucose tolerance test and resulting AUC in 16-week-old male mice (n = 5 for wild-type and n = 7 for KO mice). h Insulin tolerance test and AUC in 17-week-old male mice (n = 5 for wild-type and n = 7 for KO mice). i Normalized daily food intake of 16-week-old male mice on NCD (n = 7 for wild-type and n = 8 for KO mice). j Daily food intake in 16-week-old mice during leptin challenges (n = 6 for wild-type and n = 7 for KO mice). k Serum leptin levels in 17-week-old mice (n = 7 for wild-type and n = 6 for KO mice). l–o Metabolic analysis of 16-week-old mice (n = 6). l O2 consumption, m CO2 consumption, n energy expenditure, and o locomotor activity. Data are presented as the means ± s.e.m. Two-sample t-tests were performed for statistical analysis. *P < 0.05, ***P < 0.001.
