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. Author manuscript; available in PMC: 2019 Jan 9.
Published in final edited form as: Cell Metab. 2018 Jan 9;27(1):180–194.e6. doi: 10.1016/j.cmet.2017.12.005

Figure 1. UCP1 independent regulation of adipose fibrosis by PRDM16.

Figure 1

(A) Glucose tolerance test in Prdm16 Tg mice and the littermate controls (left) and in Ucp1−/−mice and Prdm16 Tg x Ucp1−/−mice (right) at 22°C. Mice were under HFD for 10 weeks. n= 7–8. * P<0.05, ** P<0.01.

(B) Hydroxyproline content in the BAT, the inguinal WAT and the epididymal WAT of mice with indicated genotypes under HFD for 14 weeks. n=6–10.

(C) Masson’s trichrome staining in the epididymal WAT of mice with indicated genotypes under HFD. Arrowheads indicate crown-like structures. Scale bars = 100 μm.

(D) Immunohistochemical staining with anti-mouse endotrophin antibody in the epididymal WAT of mice in (C). Arrowheads indicate crown-like structures. Scale bars = 100 μm.

(E) Expression profiles of pro-fibrotic genes (as indicated) in the inguinal WAT of mice with indicated genotypes under HFD for 14 weeks. The color scale shows z-scored FPKM representing the mRNA level of each gene in blue (low expression)-white-red (high expression) scheme. * P<0.05 by transgenic PRDM16 expression both in wild-type background and Ucp1−/− background.

(F) Cold-induced changes in gene expression of pro-fibrosis genes (% change relative to ambient temperature) in the inguinal WAT from wild-type (white) and Ucp1−/− mice (blue). Mice under 14 weeks of HFD were kept under ambient temperature or mild cold temperature at 16°C for 10 days. n=4–6. Data in A, B, and F are represented as mean ± SEM.