Association study of apelin-APJ system genetic polymorphisms with incident metabolic syndrome in a Chinese population: a case-control study
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Meijin Zhang1, Feng Peng2, Liming Lin3, Mingzhong Yu4, Chengyuan Huang5, Dan Hu6, Qinghui Guo1, Changsheng Xu7 and Jinxiu Lin2
1The First Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China
2Department of Cardiology, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China
3Department of Cardiology, The Affiliated Hospital of Putian University, Putian, Fujian, China
4Department of Cadre Ward, The First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian, China
5Department of Neurology, Zhangzhou Affiliated Hospital of Fujian Medical University, Zhangzhou, Fujian, China
6Department of Pathology, Fujian Provincial Cancer Hospital, The Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China
7Fujian Provincial Institute of Hypertension, Fuzhou, Fujian, China
Feng Peng, email: [email protected]
Jinxiu Lin, email: [email protected]
Keywords: apelin; APJ; metabolic syndrome; single nucleotide polymorphism
Received: May 27, 2017 Accepted: December 03, 2017 Epub: January 10, 2018 Published: June 04, 2019
Objectives: Apelin-APJ system has been implicated in the regulation of metabolic homeostasis. This study aimed to explore the genetic predisposition of the apelin-APJ system to metabolic syndrome.
Materials And Methods: 1005 subjects were enrolled, including 448 metabolic syndrome patients and 557 controls. Seven single nucleotide polymorphisms, including rs909656, rs5975126, and rs3115757 of the apelin gene and rs7119375, rs10501367, rs9943582 and rs11544374 of the APJ gene, were genotyped.
Results: For males, apelin-36 were higher in metabolic syndrome subjects compared with controls (p < 0.05). Apelin-36 were significantly lower in those with TT genotype of rs10501367 than those with CC and CT genotypes (p < 0.05), and fasting plasma glucose were higher in T allele carriers of rs10501367 and A allele carriers of rs7119375 compared with non-carriers (both p < 0.05). A significant difference in genotype distribution between diabetes mellitus patients and controls existed for both rs10501367 and rs7119375 (both p < 0.05). However, the association between apelin-APJ system genetic polymorphisms and metabolic syndrome was nonsignificant.
For females, apelin-36 were higher in metabolic syndrome subjects compared with controls (p < 0.05). The association between apelin-APJ system genetic polymorphisms and apelin-36, fasting plasma glucose and diabetes mellitus was nonsignificant. However, carrying A allele in rs7119375 was associated with lower metabolic syndrome risk compared with non-carriers of A allele (odds ratio: 0.646, 95% confidence interval: 0.420–0.994, p = 0.043).
Conclusions: The current findings revealed a gender-specific association of apelin-APJ system genetic polymorphisms with metabolic syndrome and glucose homeostasis disorders in a Han Chinese population.
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