Gasdermin D Deficiency Does Not Protect Mice from High-Fat Diet-Induced Glucose Intolerance and Adipose Tissue Inflammation

Figure 5

PPARγ and gasdermin D (GSDMD) expression in 3T3-L1 cells during adipogenesis. (a) Real-time PCR analysis of PPARγ genes in adipose tissue of wild-type (WT) and GSDMD KO mice fed a normal chow diet (NCD) or high-fat diet (HFD). (b) Representative western blot image and quantitative analysis of PPARγ in adipose tissue of WT and GSDMD KO mice. (c and d) Real-time PCR analysis of PPARγ and GSDMD genes during adipogenesis. (e) Representative western blot image and quantitative analysis of GSDMD protein during adipogenesis. Samples were taken before and 2, 4, and 6 days after treatment of 3T3-L1 preadipocytes with differentiation media. (f) Correlation analysis between GSDMD and PPARγ genes during adipogenesis. Protein expression levels were normalized to β-actin. Gene expression levels were normalized to 18S rRNA. vs. same genotype mice fed a NCD, ^† vs. WT NCD group, ^# vs. WT HFD group, and ^ǂ vs. D+0.

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