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. Author manuscript; available in PMC: 2018 Mar 13.
Published in final edited form as: Obesity (Silver Spring). 2016 Nov 2;25(1):155–165. doi: 10.1002/oby.21701

Figure 6. The amount of macrophage crown-like structures (CLSs) and pro-inflammatory gene transcripts were less in OCA-treated Wt mouse adipose compartments than untreated in Wt but not foz/foz mice.

Figure 6

(A) Number of adipose CLSs, and mRNA expression of (B) C-C motif chemokine receptor 2 (Ccr2), and (C) Cd11c in stromal vascular fractions (SVFs) of atherogenic diet-fed foz/foz mice vs. Wt adipose compartments, with or without OCA treatment. The ratio of alternatively-activated, anti-inflammatory macrophage markers were increased in OCA-treated Wt mouse adipose compartments vs. untreated; OCA failed to alter adipose macrophage polarization in foz/foz mice. (D) Cd68 mRNA expression, and the ratio of (E) Cd163, (F) arginase 1 (Ag1), and (G) antigen resistin-like molecule α (Fizz1) mRNA to Cd68 expression in SVFs of atherogenic diet-fed foz/foz mice vs. Wt adipose compartments, with or without OCA treatment. Data are mean ± SEM (n=9-10/gp). *P<0.05 vs. genotype-matched control (treatment effect), δP<0.05 vs. treatment-matched control (genotype effect).