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. 2001 Oct 1;108(7):1001–1013. doi: 10.1172/JCI12864

Figure 8.

Figure 8

The combination of leptin deficiency and decreased effects of PPARα pathways results in insulin resistance in heterozygous PPARγ-deficient mice without WAT induced by treatment with an RXR antagonist or a PPARγ antagonist (a and c). Amounts of the mRNAs of FAT/CD36, SREBP1, SCD1, ACO, and UCP2 in the liver (a) and in skeletal muscle (c). (b and d) TG content of the livers (b) and skeletal muscles (d) of wild-type (WT) and heterozygous PPARγ-deficient mice (+/–) untreated (–) or treated with HX531 or BADGE for 4 weeks (a–d) while on the HF diet. (e) Serum leptin levels (left) and insulin resistance index (right) of heterozygous PPARγ-deficient mice (PPARγ+/–) untreated (–) or treated with HX531 (+) for 6 weeks or PPARγ+/– treated with low doses of leptin (Lep1X), high doses of leptin (Lep10X), Wy-14,643 (Wy), or a combination for the last 12 days of a 6-week HX531 treatment while on the HF diet. HX531 or Wy-14,643 was given as a 0.1 or 0.01% food admixture, respectively. The results are expressed as the percentage of the value of untreated PPARγ+/– on the HF diet (right). HX531 or Wy-14,643 was given as a 0.1 or 0.01% food admixture, respectively. Each bar represents the mean ± SE (n = 5–10). *P < 0.05, **P < 0.01, untreated versus treated with HX531, Lep1X, Lep10X, or Wy, or compared with untreated wild-type mice. NS, no significant difference.