Regulation and function of L-PGDS in models of altered PPARγ activity.

<p>A) <i>L-PGDS</i> mRNA levels in the major metabolic tissues of <i>PPARγ2</i> KO mice. B) Body weights of all four genotypes from the <i>L-PGDS</i> x <i>PPARγ2</i> (DKO) double cross. C) DKO mice have reduced BAT mass compared to other genotypes. Both <i>PPARγ2</i> KO and DKO mice have reduced epididymal fat mass. D) DKO mice have impaired glucose tolerance compared to any other genotype. Statistics performed on area-of-curve. (Box, AOC 0–10 minutes). E) DKO mice are more insulin resistant than WT mice Statistics performed on area- of-curve. F) Serum Free fatty acid, triglyceride and insulin levels. All mice n = 8 per group C57Bl/6 males 4 months old, except mice undergoing ITT which were 4.5 months of age. *, P<0.05 <b>a</b>, P<0.05 WT vs PPARγ2, <b>b</b>, P<0.05 WT vs DKO <b>c</b>, P<0.05 PPARγ2 vs DKO, <b>d</b> P<0.05 L-PGDS vs DKO.