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. 2006 Feb 21;103(9):3444–3449. doi: 10.1073/pnas.0511253103

Fig. 1.

Fig. 1.

Depressed metabolism and glucose intolerance in PPARδ null mice. Metabolic parameters of wild-type and PPARδ null mice were measured in metabolic cages (n = 8). PPARδ null mice ate and drank less (A), consumed and produced less O2 and CO2 (B), expended less energy (presented as heat) (C), and have lower RERs (RER = VCO2/VO2) (D), particularly in the fed state (6 p.m. to 6 a.m.). (E) The glucose-tolerance test (GTT), showing that PPARδ null animals were glucose-intolerant on normal chow. (F) The GTT, showing a receptor-dependent effect of a PPARδ agonist (GW) on improving glucose tolerance. Both wild-type and PPARδ−/− mice were placed on a high-fat high-carbohydrate diet for 10 weeks, followed by a 2-week ligand treatment (n = 4). Statistical differences were observed only between vehicle- and ligand (GW)-treated wild-type mice. ∗, P < 0.05.