Peroxisome proliferator-activated receptor gamma (PPARγ) is member of a family of nuclear receptors that interacts with nuclear proteins acting as coactivators and corepressors. The colon is a major tissue which expresses PPARγ in epithelial cells and, to a lesser degree, in macrophages and lymphocytes and plays a role in the regulation of intestinal inflammation. Indeed, both natural and synthetic PPARγ ligands have beneficial effects in different models of experimental colitis, with possible implication in the therapy of inflammatory bowel disease (IBD). This paper will specifically focus on potential role of PPARγ in the predisposition and physiopathology of IBD and will analyze its possible role in medical therapy. 1. Introduction The peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor highly expressed in adipose tissue but also intestine, playing a key role in regulation of insulin resistance and inflammation. Recently its role in intestinal diseases, especially colon cancer and intestinal inflammation, is emerging. The discovery that it is the major functional receptor mediating the aminosalicylate activities in inflammatory bowel diseases (IBD) has further enhanced the interest for the role of this receptor in the regulation of gut homeostasis, with possible implication for newer therapeutic targeting. After an extensive search of medical literature in English language from the PubMed database, we aim in this paper to focus on potential role of PPARγ in the predisposition and physiopathology of IBD and to analyze its role in experimental colitis and potential therapy for IBD. 2. IBD and PPARγ: Friend or Foe The inflammatory bowel diseases (IBD), Crohn’s disease (CD), and ulcerative colitis (UC) are common causes of gastrointestinal illness characterised by chronic, relapsing intestinal inflammation, often presenting in early childhood [1]. The incidence varies according to geographical location and in Northern Europe IBD may affect upto one in two hundred of the population [2]. The division into CD and UC is made on the basis of clinical, radiological, endoscopic, and histological features. Common clinical features of CD include abdominal pain, diarrhea, weight loss, and fever. Rectal blood loss is not always a feature and up to 10% of patients with CD may not have diarrhea. Inflammatory changes are patchy in distribution and may occur anywhere within the gastrointestinal tract from the mouth to the anus. Approximately 40% of patients with CD will have disease involving both small and large bowel, in 30% the disease is
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