Lack of adipocyte FAM20C improves whole body glucose homeostasis

Figures

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  FIGURE 1. FAM20C was increased in adipose tissue with obesity. (a, b) Gene expression levels in epididymal white adipose tissue (eWAT) and subcutaneous white adipose tissue (subWAT) of mice fed an HFD. (c) Gene expression after HFD fed under indicated time. (d, e) The gene expression levels in the eWAT and subWAT of ob/ob mice compared to control mice. (f, g) Western blot analysis of FAM20C expression in eWAT of 12 weeks fed HFD or ob/ob mice relative to normal chow diet‐fed mice. (h, i) eWAT section from 12 weeks HFD fed mice or ob/ob mice and normal chow diet was stained with anti‐FAM20C antibody. Scale bars: 100 μm. Data are showed as mean ± SEM. *p < 0.05, **p < 0.01.

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  FIGURE 2. Adipose‐specific FAM20C deletion protects mice to obesity, impaired adipose tissue expansion. (a) qPCR analysis of FAM20C mRNA expression in adipose tissue from mice. (b) Western blot analysis of FAM20C protein level in tissues and mature adipocyte from control and KO mice. (c) Body weight of control and KO mice fed an NCD and HFD. (d) Representative pictures of control and KO mice. (e) Representative WAT pictures of control and KO mice. (f) Weight of adipose tissue including eWAT, subWAT and BAT. (g) Food intake. (h) Water intake. (i) Hematoxylin and eosin staining of eWAT, subWAT and BAT of NCD fed control and KO mice. Scale bar = 100 μm. (j) Hematoxylin and eosin staining of eWAT, subWAT and BAT of HFD‐fed control and KO mice. Scale bar = 100 μm. (k) eWAT adipocyte size of control and KO mice. (l) subWAT adipocyte size of control and KO mice. Data are represented as mean ± SEM. *p < 0.05, **p < 0.01.

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  FIGURE 3. Adipose‐specific FAM20C deletion ameliorates insulin resistance. (a) Blood glucose concentrations during glucose tolerance tests from HFD fed mice. (b) Blood glucose concentrations during insulin tolerance tests from HFD fed mice. (c) Fasting blood glucose and (d) insulin concentration after 12 weeks HFD feeding. (e) Serum adiponectin and (f) leptin concentration after 12 weeks HFD feeding. Data are represented as mean ± SEM. *p < 0.05.

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  FIGURE 4. Adipose‐specific FAM20C deletion increase energy expenditure. (a–h) Indirect calorimetry analysis. VO2: Rate of oxygen consumption; VCO2: Rate of carbon dioxide production. EE: Energy expenditure; RER: Respiratory exchange ratio; n = 6/group. (i, j) Monitoring of food intake and water intake. Data are represented as mean ± SEM. *p < 0.05.

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  FIGURE 5. HFD‐fed adipocyte‐specific FAM20C KO mice ameliorates hepatosis. (a) Hematoxylin and eosin sections of liver tissues from NCD and HFD mice. Scale bar: 100 μm. (b) Oil‐red O staining of liver tissues from HFD‐induced mice. Scale bar: 100 μm. (c) liver weight from HFD fed control and KO mice. (d) Hepatic triglycerides level in livers of control and KO mice fed an HFD. (e) Level of serum Triglyceride and (f) total cholesterol from control and KO HFD‐fed mice. Data are represented as mean ± SEM. *p < 0.05, **p < 0.01.

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  FIGURE 6. Gene profile of WAT from HFD‐fed adipocyte‐specific FAM20C KO mice and control mice. (a) The principal components analysis (PCA) (b, c) Heatmap and volcano plot analysis of RNA sequence in WAT of FAM20C KO and control mice; n = 4/group. (d, e) KEGG pathway analysis of differentially expressed genes (DEGs) of FAM20C KO mice and control mice. (f, g) Gene Set Enrichment Analysis (GSEA) identifying the significantly downregulated pathways.

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  FIGURE 7. Deletion of FAM20C in adipocyte ameliorates collagen deposition and macrophage infiltration in adipose tissue. (a, b) Immunohistochemistry for F4/80 in eWAT and subWAT from NCD or HFD‐fed control and KO mice and quantification, Scale bar = 100 μm. (c, d) qPCR analysis of inflammatory genes in adipose tissue from eWAT and subWAT of HFD‐fed mice. (e, f) Trichrome staining for collagen deposition in eWAT and subWAT from NCD or HFD‐fed control and KO mice. Data are represented as mean ± SEM. *p < 0.05, **p < 0.01.