Figure 2.

Adipocyte-selective RXRα ablation in mice. (A) Efficiency of RXRα inactivation in adipocytes. Cre-ER^T2-mediated RXRα disruption was analyzed by Southern blotting DNA extracted from WAT (T) isolated from 4-month-old aP2-Cre-ER^T2(tg/0)/RXRα^L2/− mice, 3 months after vehicle (−) and Tam (+) treatments, and from the supernatant (S) and pellet (P) fractions after centrifugation of collagenase-treated WAT. Positions of RXRα L2, L−, and (−) alleles are indicated. (B) Expression of nuclear receptors, PPARγ target genes, and Pref-1 in RXRα-deficient adipose tissue. RXRβ, RXRγ, PPARγ, aP2, and LPL mRNA levels were analyzed by Northern blotting RNA isolated from WAT of 6-month-old CT (lanes 1, 3, and 5) and RXRα^adL−/− (KO, lanes 2, 4, and 6) mice, under RD (lanes 1 and 2), after MSG treatment (lanes 3 and 4) and under HFD (lanes 5 and 6). 36B4 was used as an internal control. Pref-1 expression was analyzed by RT-PCR performed on the same RNA samples, and HPRT was used as an internal control. (C) Altered RXRγ and aP2 expression in the adipose tissue of RXRα^adL−/− mice 2 weeks after Tam injection. RXRγ and aP2 mRNA levels were analyzed by Northern blotting RNA isolated from adipose tissue of two 6-week-old CT (lanes 1 and 2) and RXRα^adL−/− (KO, lanes 3 and 4) mice, 2 weeks after Tam treatment. 36B4 was used as an internal control.