Abstract
Type 2 diabetes mellitus is characterized by insulin resistance as well as progressive pancreatic β-cell dysfunction. Thiazoli dinediones (TZDs) are a class of hypoglycemic medications that influence insulin sensitivity in peripheral tissue [1]. Piogl itazone is a TZD, peroxisome proliferator-activated receptor (PPAR)-γ ligand used in the treatment of type 2 diabetic patients [2]. Many preclinical trials have demonstrated that PPAR-γ is a potential molecular target for the development of bladder cancer. Yoshimura et al. [3] found PPAR-γ mRNA in bladder cancer samples. Furthermore, immunohistochemistry revealed that the protein expression of PPAR-γ was significantly higher with increasing grade and increasing stage of bladder cancer [3]. In male rats exposed to muraglitazar, a dual human PAPR-α/γ agonist, there was a dose-related increased incidence of transitional cell papilloma and carcinoma of the urinary bladder [4]. Lubet et al. [5] also reported that another PPAR-γ agonist, rosiglitazone, enhanced bladder tumors in rats pretreated with N-(4-hydroxybutyl)-N-(butyl)-nitrosamine (BBN), a known DNA-reactive bladder carcinogen in several species. However, the mechanisms underlying this pro-tumor potential of pioglitazone for bladder cancer are not fully understood. In the large prospective pioglitazone clinical trial in macrovascular events (PROactive) study, 14 bladder cancers occurred in the pioglitazone arm (0.5%) versus 6 in the placebo arm (0.2%) [6], and in September 2010, the U.S. Food and Drug
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