Atug Ozlen, Tahan Veysel, Eren Fatih, Tiftikci Arzu, Imeryuz Nese, Hamzaoglu Hulya Over, Tozun Nurdan
Marmara University School of Medicine, Department of Gastroenterology, Istambul, Turkey.
J Gastrointestin Liver Dis. 2008 Dec;17(4):433-7.
BACKGROUND & AIMS: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) has recently been implicated as an endogenous regulator of cellular proliferation and inflammation. Impaired expression of PPAR-gamma in colonic epithelial cells in ulcerative colitis (UC) and increased expression in hypertrophic mesenteric adipose tissue in Crohn's disease (CD) have been reported. Furthermore, PPAR-gamma ligands have been shown to inhibit tissue injury associated with immune activation in UC. Any mutation in PPAR-gamma gene may be responsible for the increase in inflammatory mediators and hence the perpetuation of inflammation in inflammatory bowel disease (IBD) patients. One common polymorphism in PPAR-gamma gene is proline to alanine substitution (Pro12Ala) which results from a CCA to GCA missense substitution in codon 12 of exon 2 of the PPAR-gamma gene. In this study, we aimed to explore Pro12Ala polymorphism in PPAR-gamma gene in IBD in Turkish patients.
69 patients with CD, 45 with UC and 100 controls of similar age and sex were studied. Genomic DNA was isolated from peripheral blood leucocytes and mutagenically separated-polymerase chain reaction (PCR) analyses were performed to determine the Pro12Ala polymorphism of the PPAR-gamma gene.
We observed no significant differences in the frequency of the Pro12Ala polymorphism in the PPAR-gamma gene among subjects with CD, UC and controls (15.9%, 15.5% and 13%, respectively, p>0.05).
These results suggest that Pro12Ala polymorphism in the PPAR-gamma gene relates neither to the risk of the development of inflammatory bowel disease nor to the clinical subtypes of CD in the Turkish population.
过氧化物酶体增殖物激活受体γ（PPAR-γ）最近被认为是细胞增殖和炎症的内源性调节因子。据报道，溃疡性结肠炎（UC）患者结肠上皮细胞中PPAR-γ表达受损，而克罗恩病（CD）患者肥厚的肠系膜脂肪组织中PPAR-γ表达增加。此外，PPAR-γ配体已被证明可抑制UC中与免疫激活相关的组织损伤。PPAR-γ基因的任何突变都可能导致炎症介质增加，从而导致炎症性肠病（IBD）患者炎症持续存在。PPAR-γ基因的一种常见多态性是脯氨酸到丙氨酸的替代（Pro12Ala），它是由PPAR-γ基因第2外显子第12密码子中的CCA到GCA错义替代引起的。在本研究中，我们旨在探讨土耳其IBD患者PPAR-γ基因中的Pro12Ala多态性。
研究了69例CD患者、45例UC患者和100例年龄和性别相似的对照者。从外周血白细胞中分离基因组DNA，并进行诱变分离聚合酶链反应（PCR）分析，以确定PPAR-γ基因的Pro12Ala多态性。
我们观察到，CD患者、UC患者和对照者中PPAR-γ基因Pro12Ala多态性的频率没有显著差异（分别为15.9%、15.5%和13%，p>0.05）。
这些结果表明，PPAR-γ基因中的Pro12Ala多态性与土耳其人群中炎症性肠病的发生风险以及CD的临床亚型均无关。
