Fig. 3: The Adamts14−/− mice showed resistance to weight gain and altered adipose histomorphology under HFD conditions. | Nature Communications

Fig. 3: The Adamts14−/− mice showed resistance to weight gain and altered adipose histomorphology under HFD conditions.

From: Large scale phenotype imputation and in vivo functional validation implicate ADAMTS14 as an adiposity gene

Fig. 3: The Adamts14−/− mice showed resistance to weight gain and altered adipose histomorphology under HFD conditions.

a Body weight increase of WT and homozygous-null animals, starting at 2 months old and through the 13 weeks of HFD exposure. Data expressed as mean ± s.e. and analysed in a linear mixed model with repeated measures. N = 8 per genotype initially, down to 6 Adamts14+/+ and 7 Adamts14−/− by week 13. Extended data can be found in Supplementary Data 11. b Cumulative frequency distribution of adipocyte cell-surface area for the gluteofemoral and gonadal fat pads, compared between the two genotypes using a two-sided Kolmogorov–Smirnov test (P = 1.376 × 10−6 for gluteofemoral fat and <2.2 × 10−16 for gonadal fat). The inset shows the total number of cells (expressed as mean ± s.e.) and violin plots for the proportional adipocyte size distributions with the overall means for the two genotypes. N = 6 Adamts14+/+ and 7 Adamts14−/− and at least 3 independent images quantified per fat pad per animal. Significance denoted as * for P < 0.05, ** for P < 0.01 and *** for P < 0.001. Extended data can be found in Supplementary Data 13.

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