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CTNNB1/β-catenin dysfunction contributes to adiposity by regulating the cross-talk of mature adipocytes and preadipocytes

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Academic year: 2020

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Figure

Fig. 1. Genetic mutations in the CTNNB1 gene are associated with human obesity. (A) Comparison of the low-frequency CTNNB1 mutations in control and obese subjects
Fig. 2. -Catenin was induced in the development of obesity in humans and mice. (A) -catenin expression was significantly higher in subcutaneous adipose tissue of obese subjects than in lean subjects
Fig. 3. Ablation of white adipose tissue. Data are shown as mean ± SEM. *in mature adipocytes and SVF cells from brown adipose tissues (BAT), iWAT, and eWAT between chow diet–fed control and ABKO mice (weight curve of control and ABKO mice under chow diet
Fig. 4. Ablation of -catenin in mature adipocyte improves metabolic homeostasis. (A) Glucose tolerance test after 16-hour fasting in 24-week HFD-fed control and ABKO mice (n = 13 for each group)
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