dc.contributor.author |
Bayrak, Tulin |
|
dc.contributor.author |
Dursun, Polat |
|
dc.contributor.author |
Bayrak, Ahmet |
|
dc.contributor.author |
Gultekin, Murat |
|
dc.contributor.author |
Kolusari, Ali |
|
dc.contributor.author |
Cakir, Erdinc |
|
dc.contributor.author |
Ozyurt, Merve |
|
dc.contributor.author |
Zeyneloglu, Hulusi B. |
|
dc.date.accessioned |
2024-03-26T07:24:38Z |
|
dc.date.available |
2024-03-26T07:24:38Z |
|
dc.date.issued |
2012 |
|
dc.identifier.citation |
Bayrak, 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/10.3109/09513590.2012.683068 |
en_US |
dc.identifier.issn |
0951-3590 |
|
dc.identifier.issn |
1473-0766 |
|
dc.identifier.uri |
http://dx.doi.org/10.3109/09513590.2012.683068 |
|
dc.identifier.uri |
https://www.webofscience.com/wos/woscc/full-record/WOS:000309938700011 |
|
dc.identifier.uri |
http://earsiv.odu.edu.tr:8080/xmlui/handle/11489/5303 |
|
dc.description |
WoS Categories: Endocrinology & Metabolism; Obstetrics & Gynecology |
en_US |
dc.description |
Web of Science Index: Science Citation Index Expanded (SCI-EXPANDED) |
en_US |
dc.description |
Research Areas: Endocrinology & Metabolism; Obstetrics & Gynecology |
en_US |
dc.description.abstract |
Objective: 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.iso |
eng |
en_US |
dc.publisher |
TAYLOR & FRANCIS LTD-ABINGDON |
en_US |
dc.relation.isversionof |
10.3109/09513590.2012.683068 |
en_US |
dc.rights |
info:eu-repo/semantics/openAccess |
en_US |
dc.subject |
PCOS, PON1, homocysteine thiolactonase, ADMA, PAF-AH, atherosclerotic heart disease |
en_US |
dc.subject |
POLYCYSTIC-OVARY-SYNDROME, OXIDE SYNTHASE INHIBITOR, SERUM PARAOXONASE, RISK-FACTOR, MYOCARDIAL-INFARCTION, INSULIN-RESISTANCE, DIABETES-MELLITUS, PLASMA, ATHEROSCLEROSIS, DISEASE |
en_US |
dc.title |
Paraoxonase lactonase activity (PON-HTLase), asymmetric dimethylarginine (ADMA) and platelet activating factor-acetylhydrolase (PAF-AH) activity in non-obese women with PCOS |
en_US |
dc.type |
article |
en_US |
dc.relation.journal |
GYNECOLOGICAL ENDOCRINOLOGY |
en_US |
dc.contributor.department |
Ordu Üniversitesi |
en_US |
dc.contributor.authorID |
0000-0002-4221-4459 |
en_US |
dc.contributor.authorID |
0000-0002-0289-2642 |
en_US |
dc.contributor.authorID |
0000-0001-5139-364X |
en_US |
dc.identifier.volume |
28 |
en_US |
dc.identifier.issue |
11 |
en_US |
dc.identifier.startpage |
874 |
en_US |
dc.identifier.endpage |
878 |
en_US |