Correlation between PPARg2 gene Pro12Ala polymorphism and cerebral infarction in an Inner Mongolian Han Chinese population

Abstract

ABSTRACT. The variant of PPAR-g2 has been shown to promote the increase of carotid IMT in patients suffering from cerebral infarction and the Pro12Ala polymorphism in the peroxisome proliferatoractivated receptorg2 (PPARg2) gene may be associated with cerebral infarction. However, due to the different genetic background, race, and regional variations of cerebral infarction patient, the results of investigations into this subject differ. The aim of this study was to investigate this polymorphism in relation to cerebral infarction among the Inner Mongolian Han Chinese population. A total of 574 Han Chinese individuals from Inner Mongolian were selected randomly, including 302 patients with cerebral infarction and 272 healthy controls. Polymerase chain reaction-restriction fragment length polymorphism was used to determine genotypes of the PPARg2 Pro12Ala variant and results were confirmed by direct sequencing. Genotype frequencies were found to be 90.7 and 91.9% for P/P, 8.6 and 7.7% for P/A, and 0.7 and 0.4 for A/A in the cerebral infarction and control groups, respectively. No statistically significant differences in genotype distribution were observed between the two groups (P > 0.05). Moreover, PPARg2 Pro12Ala genotype was not significantly associated with altered fasting blood glucose, blood pressure, or serum lipid profiles. After adjustment for gender, body mass index, and smoking habit, logistic regression was used to analyze the relationship between the Pro12Ala polymorphism and cerebral infarction (odds ratio = 0.888, 95% confidence interval = 0.106-7.460, P > 0.05), revealing that this variant was not the main pathogenic factor involved. Therefore, the Pro12Ala mutation of PPARg2 may not be associated with cerebral infarction in the Inner Mongolian Han Chinese population.

Relationship between PPAR‐γ gene polymorphisms and ischemic stroke risk: A meta‐analysis

“…After the full‐text review, 64 studies were excluded further (overlapping data [ n = 2], other polymorphism loci [ n = 3], reviews [ n = 3], irrelevant studies [ n = 16], and biology studies [ n = 38]) (Figure 1). Finally, 16 studies involving 3786 patients and 5343 controls were included in this meta‐analysis (Bazina et al., 2015; Chehaibi et al., 2014; L. Huang et al., 2007; Lee et al., 2007, 2006; X. Li et al., 2016; Z. J. Liu et al., 2010; Lu et al., 2009; Shen & Ha, 2005; Sun, 2010; Tong et al., 2015, 2016; Wang et al., 2019; Wei et al., 2013; Yuan, 2008; Zafarmand et al., 2008). Of these, 10 case–control studies focused on rs1801282 C/G polymorphism (Bazina et al., 2015; L. Huang et al., 2007; Lee et al., 2006, 2007; X. Li et al., 2016; Shen & Ha, 2005; Tong et al., 2015, 2016; Wang et al., 2019; Zafarmand et al., 2008) and, seven case–control studies focused on rs3856806 C/T polymorphism (Chehaibi et al., 2014; Z. J. Liu et al., 2010; Lu et al., 2009; Sun, 2010; Wang et al., 2019; Wei et al., 2013; Yuan, 2008).…”

“…Finally, 16 studies involving 3786 patients and 5343 controls were included in this meta-analysis (Bazina et al, 2015;Chehaibi et al, 2014;L. Huang et al, 2007;Lee et al, 2007Lee et al, , 2006X. Li et al, 2016;Z.…”

“…Of these, 10 case-control studies focused on rs1801282 C/G polymorphism (Bazina et al, 2015;L. Huang et al, 2007;Lee et al, 2006Lee et al, , 2007X. Li et al, 2016;Shen & Ha, 2005;Tong et al, 2015Tong et al, , 2016Wang et al, 2019;Zafarmand et al, 2008) and, seven case-control studies focused on rs3856806 C/T polymorphism (Chehaibi et al, 2014;Z.…”

Association Between Ghrelin Gene Polymorphism and Cerebral Infarction

“…Studies have demonstrated that multiple gene polymorphisms affect the occurrence of cerebral infarction. For example, CTSS gene [ 8 ] and PPARG2 gene [ 9 ] polymorphisms are associated with the occurrence of cerebral infarction in the Chinese population, and the ALDH2 gene polymorphism affects the collateral circulation and prognosis of cerebral infarction patients [ 10 ]. As the ligand for the growth hormone secretagogue receptor, the ghrelin gene promotes the release of growth hormone, thereby affecting various biological functions.…”