Liver-specific disruption of PPARγ in leptin-deficient mice improves fatty liver but aggravates diabetic phenotypes
J. Clin. Invest. Kimihiko Matsusue, et al. 111:737 doi:10.1172/JCI17223 [Go to this article.]

Figure 3
Northern blot analysis to assess the effect of PPARγ deficiency on hepatic gene expression in untreated and rosiglitazone-treated ob/ob mice. Total RNA was isolated from nonfasting male mice and 20 μg was subjected to electrophoresis on a 1.2% agarose gel, transferred to a nylon membrane, and hybridized with the indicated ³²P-labeled cDNA probes. (a) Northern blot of untreated ob/ob mice liver. (b) Northern blots of rosiglitazone-treated ob/ob mice liver. Quantitation of the bands was performed using the PhosphorImager from Molecular Dynamics and are expressed as the fold change, after correction for GAPDH levels, relative to OB/OB-PPARγ(fl/fl)AlbCre^– mice. Values are averages obtained from two animals.