Activation of PPAR by Rosiglitazone Does Not Negatively Impact Male Sex Steroid Hormones in Diabetic Rats
Figure 1
(a) Real-time PCR analysis of testicular PPAR mRNA levels in lean nondiabetic controls (Lean C), Zucker diabetic fatty (ZDF) untreated (Diabetic U), and ZDF rats treated with rosiglitazone (Diabetic T). Data are expressed as mean SE. per group, . (b) Agarose gel (2%) showing real-time PCR products generated in (a). Lane 1, DNA markers, lanes 2-3, RNA templates (instead of cDNA) from fat (-VF) and prostate (-VPr) as negative controls. Lanes 4-5, fat from untreated rats (FU) and prostate (Pr) as positive controls. Lanes 6–9, testicular PCR products from RNA negative controls (-VT), diabetic treated (DT), Diabetic untreated (DU), and lean untreated (LU) rats. Lane 10, fat from ZDF-treated rats (FT). (c) Representative IHC of PPAR protein in the testis of DT (panel 2a with insert box magnified in 2b), DU (panel 3), and LU rats (panel 4). Panel 1, -VT = negative control testis section (minus primary antibody. Arrows indicate PPAR localization in spermatogonia and in Leydig cells.
