Please use this identifier to cite or link to this item: http://earsiv.odu.edu.tr:8080/xmlui/handle/11489/5303
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dc.contributor.authorBayrak, Tulin-
dc.contributor.authorDursun, Polat-
dc.contributor.authorBayrak, Ahmet-
dc.contributor.authorGultekin, Murat-
dc.contributor.authorKolusari, Ali-
dc.contributor.authorCakir, Erdinc-
dc.contributor.authorOzyurt, Merve-
dc.contributor.authorZeyneloglu, Hulusi B.-
dc.date.accessioned2024-03-26T07:24:38Z-
dc.date.available2024-03-26T07:24:38Z-
dc.date.issued2012-
dc.identifier.citationBayrak, T., Dursun, P., Bayrak, A., Gültekin, M., Kolusari, A., Çakir, E., Ozyurt, M., Zeyneloglu, HB. (2012). Paraoxonase lactonase activity (PON-HTLase), asymmetric dimethylarginine (ADMA) and platelet activating factor-acetylhydrolase (PAF-AH) activity in non-obese women with PCOS. Gynecol. Endocrinol., 28(11), 874-878. https://doi.org/10.3109/09513590.2012.683068en_US
dc.identifier.issn0951-3590-
dc.identifier.issn1473-0766-
dc.identifier.urihttp://dx.doi.org/10.3109/09513590.2012.683068-
dc.identifier.urihttps://www.webofscience.com/wos/woscc/full-record/WOS:000309938700011-
dc.identifier.urihttp://earsiv.odu.edu.tr:8080/xmlui/handle/11489/5303-
dc.descriptionWoS Categories: Endocrinology & Metabolism; Obstetrics & Gynecologyen_US
dc.descriptionWeb of Science Index: Science Citation Index Expanded (SCI-EXPANDED)en_US
dc.descriptionResearch Areas: Endocrinology & Metabolism; Obstetrics & Gynecologyen_US
dc.description.abstractObjective: Paraoxonase1 (PON1), exhibits both esterase activity (PON1-AREase) and homocysteine thiolactonase activity (PON1-HTLase) which respectively prevent LDL oxidation and detoxify homocysteine thiolactone (HTL). Platelet-activating factor-acetylhydrolase (PAF-AH) is an antioxidant enzyme preventing LDL oxidation by hydrolysis of oxidized phospholipids. Both of these enzymes exhibit a proatherogenic role. ADMA is an endogenous inhibitor of nitric oxide (NO) synthesis causing endothelial dysfunction. The aim was to compare non-obese PCOS patients with a BMI matched control group using the following characteristics: serum PON1-HTLase, ADMA, PAF-AH, and lipid and hormonal parameters. Results: 77 women with PCOS and 25 healthy subject were recruited for this study, The controls were non-obese BMI and age matched with the patients. There were no significant differences with respect to age, BMI, FSH, free testosterone, DHEA, androstenadion, total cholesterol, triglycerides, HDL, LDL, VLDL, fasting glucose/insulin ratio and HOMA-IR among the groups (p > 0.05). However, total testosterone and fasting glucose levels were significantly higher in the PCOS group (p < 0.05). On the other hand, PON1-HTLase levels (39.6 +/- 5.77 vs. 33.8 +/- 8.2, p = 0.02) were significantly lower in the PCOS group while ADMA levels (1.14 +/- 0.6 vs. 3.37 +/- 6.4, p = 0.004) were significantly higher in the PCOS group. However, there was no significant difference in PAF-AH activity among the groups Conclusions: Decreased PON1-HTLase and increased ADMA levels might be a relevant marker for the development of future atherosclerotic heart disease (AHD) in non-obese PCOS patients. Further studies are needed to confirm our results.en_US
dc.language.isoengen_US
dc.publisherTAYLOR & FRANCIS LTD-ABINGDONen_US
dc.relation.isversionof10.3109/09513590.2012.683068en_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectPCOS, PON1, homocysteine thiolactonase, ADMA, PAF-AH, atherosclerotic heart diseaseen_US
dc.subjectPOLYCYSTIC-OVARY-SYNDROME, OXIDE SYNTHASE INHIBITOR, SERUM PARAOXONASE, RISK-FACTOR, MYOCARDIAL-INFARCTION, INSULIN-RESISTANCE, DIABETES-MELLITUS, PLASMA, ATHEROSCLEROSIS, DISEASEen_US
dc.titleParaoxonase lactonase activity (PON-HTLase), asymmetric dimethylarginine (ADMA) and platelet activating factor-acetylhydrolase (PAF-AH) activity in non-obese women with PCOSen_US
dc.typearticleen_US
dc.relation.journalGYNECOLOGICAL ENDOCRINOLOGYen_US
dc.contributor.departmentOrdu Üniversitesien_US
dc.contributor.authorID0000-0002-4221-4459en_US
dc.contributor.authorID0000-0002-0289-2642en_US
dc.contributor.authorID0000-0001-5139-364Xen_US
dc.identifier.volume28en_US
dc.identifier.issue11en_US
dc.identifier.startpage874en_US
dc.identifier.endpage878en_US
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