Angiotensin II Promotes White Adipose Tissue Browning and Lipolysis in Mice

Figures

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  Figure 1. Ang II dose-dependently reduces fat mass in mice. Relative weights of (a) heart, (b) liver, (c) spleen, (d) kidney, (e) subcutaneous white adipose tissue (SWAT), (f) epididymal white adipose tissue (EWAT), (g) perirenal white adipose tissue (perirenal WAT), and (h) brown adipose tissue (BAT) in C57BL/6 mice infused with different doses of Ang II (1.44 mg/kg/d and 2.5 mg/kg/d) or saline for 2 weeks.

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  Figure 2. Ang II induces white adipose tissue (WAT) browning. (a) H&E and Ucp1 immunohistochemistry (IHC) staining in SWATs in mice infused with saline or Ang II (2.5 mg/kg/d) for 2 weeks. (b) Quantification of Ucp1-positive area in SWATs of mice from (a). (c) H&E and Ucp1 IHC staining in EWATs. (d) Quantification of Ucp1-positive area in EWATs. (e) Gene expression analysis of browning marker in EWATs.

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  Figure 3. Activation of lipolysis by Ang II treatment. (a) Triglyceride, (b) total cholesterol, (c) low-density lipoprotein cholesterol (LDL-C), and (d) high-density lipoprotein cholesterol (HDL-C) were measured in C57BL/6 mice infused with different doses of Ang II (1.44 mg/kg/d and 2.5 mg/kg/d) or saline for 2 weeks.

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  Figure 4. The effect of Ang II on WAT browning is partially mediated by Ang II type 1 receptor (AT1R). (a) H&E and Ucp1 immunohistochemistry (IHC) staining in SWATs of mice infused with saline or Ang II (2.5 mg/kg/d) for 2 weeks and treated with or without the Ang II type 1 receptor blocker valsartan. (b) Quantification of Ucp1-positive area in SWATs of mice from (a).

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  Figure 5. Transcriptomics-based screening of differential gene expression profile. (a) The heat map shows the upregulated and downregulated genes in SWATs from C57BL/6 mice infused with saline or Ang II (2.5 mg/kg/d) for 2 weeks. Each column represents an individual replicate, and n = 3 replicates for each group. Each row represents an individual gene. The color bar represents the z-score-transformed relative expression of normalized counts of genes that are upregulated and downregulated. (b) String diagram of differentially expressed genes (DEGs) based on GO functional enrichment analysis. (c) GO pathway analysis of DEGs between control and Ang II groups. (d) KEGG pathway analysis of DEGs between control and Ang II groups.

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  Figure 6. Ang II treatment enhanced AMPKα phosphorylation in adipocytes. (a, b) Western blot analyses assessing the protein expression levels of phospho-AMPKα (P-AMPKα) and AMPKα in WATs from C57BL/6 mice infused with saline or Ang II (2.5 mg/kg/d) for 2 weeks. (c) Western blot analyses assessing the protein expression levels of P-AMPKα and AMPKα in 3T3-L1 cells treated with 1 μM Ang II for the indicated time. (d) Stromal vascular fraction (SVF)/preadipocytes were isolated from SWAT of C57BL/6 mice and cultured in differentiation medium with or without Ang II treatment. Western blot analyses assessing the protein expression levels of P-AMPKα and AMPKα in these cells.