D Liao1, H Yu2, L Han3, C Zhong1, X Ran1, D Wang1, L Mo4. 1. Department of Gynaecology and Obstetrics, Dongguan Third People's Hospital, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, No. 1, Huangzhou Xianglong Road of Shilong Town, Dongguan, 523326, Guangdong, China. 2. Department of Gynaecology and Obstetrics, Dongguan Maternal and Child Health Hospital, Dongguan, China. 3. Department of Gynaecology, Dongguan Changan Hospital, Dongguan, 523560, Guangdong, China. 4. Department of Gynaecology and Obstetrics, Dongguan Third People's Hospital, Affiliated Dongguan Shilong People's Hospital of Southern Medical University, No. 1, Huangzhou Xianglong Road of Shilong Town, Dongguan, 523326, Guangdong, China. lifangmo8233@163.com.
Abstract
PURPOSE: Evidences showed that paraoxonase 1 (PON1) gene polymorphism has an impact on women's susceptibility to polycystic ovarian syndrome (PCOS) by influencing the expression and activity of PON1. However, the effects of three PON1 polymorphisms (- 108 C>T, L55M and Q192R) on the incidence of PCOS have generated inconsistent results. Here, we conducted a meta-analysis to investigate the association between PON1 polymorphisms and PCOS risk. METHODS: All eligible trials were identified via systematic searches of multiple literature databases. Outcome data were synthesized by using crude odds ratio with 95% confidence interval. Heterogeneity was assessed with the I2 test. Publication bias and subgroup analyses were also performed. RESULTS: A total of 2449 cases and 1977 controls from nine studies were selected for analysis. The pooled results showed a significant association between PCOS risk and PON1 - 108 C/T polymorphism in the following genetic models [allelic, 0.72 (0.56-0.92); homozygote, 0.51 (0.32-0.82); heterozygote, 0.44 (0.25-0.78); and dominant 0.47 (0.29-0.77)]. For the PON1 192 Q/R polymorphism, a significant relationship was found in the allelic model [0.62 (0.41-0.93)] and recessive model [0.61 (0.37-0.98)]. PCOS risk was also linked to PON1 L55M polymorphism in the heterozygote model [0.62 (0.39-0.98)] and dominant model [0.63 (0.41-0.96)]. CONCLUSIONS: Our study has shown that PON1 - 108 C/T polymorphism might be associated with increased risk of PCOS under the allelic, homozygote, heterozygote, and dominant models. Additionally, PON1 192 Q/R and L55M polymorphisms were significantly related only in the allelic and recessive model, and in the heterozygote and dominant model, respectively.
PURPOSE: Evidences showed that paraoxonase 1 (PON1) gene polymorphism has an impact on women's susceptibility to polycystic ovarian syndrome (PCOS) by influencing the expression and activity of PON1. However, the effects of three PON1 polymorphisms (- 108 C>T, L55M and Q192R) on the incidence of PCOS have generated inconsistent results. Here, we conducted a meta-analysis to investigate the association between PON1 polymorphisms and PCOS risk. METHODS: All eligible trials were identified via systematic searches of multiple literature databases. Outcome data were synthesized by using crude odds ratio with 95% confidence interval. Heterogeneity was assessed with the I2 test. Publication bias and subgroup analyses were also performed. RESULTS: A total of 2449 cases and 1977 controls from nine studies were selected for analysis. The pooled results showed a significant association between PCOS risk and PON1 - 108 C/T polymorphism in the following genetic models [allelic, 0.72 (0.56-0.92); homozygote, 0.51 (0.32-0.82); heterozygote, 0.44 (0.25-0.78); and dominant 0.47 (0.29-0.77)]. For the PON1 192 Q/R polymorphism, a significant relationship was found in the allelic model [0.62 (0.41-0.93)] and recessive model [0.61 (0.37-0.98)]. PCOS risk was also linked to PON1L55M polymorphism in the heterozygote model [0.62 (0.39-0.98)] and dominant model [0.63 (0.41-0.96)]. CONCLUSIONS: Our study has shown that PON1 - 108 C/T polymorphism might be associated with increased risk of PCOS under the allelic, homozygote, heterozygote, and dominant models. Additionally, PON1 192 Q/R and L55M polymorphisms were significantly related only in the allelic and recessive model, and in the heterozygote and dominant model, respectively.
Authors: C J Petry; K K Ong; K F Michelmore; S Artigas; D L Wingate; A H Balen; F de Zegher; L Ibáñez; D B Dunger Journal: Hum Reprod Date: 2005-03-31 Impact factor: 6.918
Authors: Gary Ginsberg; Patricia Neafsey; Dale Hattis; Kathryn Z Guyton; Douglas O Johns; Babasaheb Sonawane Journal: J Toxicol Environ Health B Crit Rev Date: 2009 Impact factor: 6.393
Authors: Bart C J M Fauser; Basil C Tarlatzis; Robert W Rebar; Richard S Legro; Adam H Balen; Roger Lobo; Enrico Carmina; Jeffrey Chang; Bulent O Yildiz; Joop S E Laven; Jacky Boivin; Felice Petraglia; C N Wijeyeratne; Robert J Norman; Andrea Dunaif; Stephen Franks; Robert A Wild; Daniel Dumesic; Kurt Barnhart Journal: Fertil Steril Date: 2011-12-06 Impact factor: 7.329
Authors: Danielle Hiam; Alba Moreno-Asso; Helena J Teede; Joop S E Laven; Nigel K Stepto; Lisa J Moran; Melanie Gibson-Helm Journal: J Clin Med Date: 2019-10-03 Impact factor: 4.241