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1.
J Assist Reprod Genet ; 34(12): 1691-1698, 2017 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-28900795

RESUMEN

PURPOSE: Proteomic studies suggest an association between haptoglobin (Hp) and polycystic ovary syndrome (PCOS). Hp is a classic inflammatory marker and binds to the intravascular hemoglobin, avoiding the oxidative damages that can be caused by free hemoglobin. Inflammation and oxidative stress are important in the pathogenesis of the PCOS, one of the most frequent metabolic diseases in women. METHODS: To validate these proteomic studies, we developed a controlled cross-sectional study that aimed to evaluate the Hp levels and allelic and genotypic frequencies of Hp1-Hp2 polymorphism in Brazilian women with PCOS. We also investigated the correlation between Hp levels and several important parameters in PCOS as follows: body mass index (BMI), waist circumference (WC), fasting glucose, post-prandial glucose, homeostatic model assessment (HOMA), lipid accumulation product (LAP), C-reactive protein (CRP), and metabolization test of tetrazolium salts (MTTs-serum antioxidant capacity). RESULTS: Plasma Hp levels were higher in the PCOS group than in controls [8.20 (4.04) g/L; 7.98 (3.31) g/L; p = 0.018]. No significant difference was observed in the frequency of Hp1-Hp2 genotypes under additive, recessive, or dominant model of inheritance between the PCOS and the control groups. Plasma Hp levels did not differ according to the genotype. However, plasma Hp showed a negative correlation with MTT (r = - 0.383; p = 0.028), as well as a positive correlation with CRP (r = 0.361; p = 0.014) in the PCOS group. CONCLUSION: Hp1-Hp2 polymorphism is not associated with PCOS but plasma Hp could be a potential biomarker for PCOS and its complications.


Asunto(s)
Biomarcadores/análisis , Haptoglobinas/genética , Haptoglobinas/metabolismo , Síndrome del Ovario Poliquístico/sangre , Síndrome del Ovario Poliquístico/genética , Polimorfismo Genético , Adolescente , Adulto , Estudios de Casos y Controles , Estudios Transversales , Femenino , Humanos , Resistencia a la Insulina , Proteómica , Adulto Joven
2.
Gene ; 644: 129-136, 2018 Feb 20.
Artículo en Inglés | MEDLINE | ID: mdl-29109005

RESUMEN

Dyslipidemia is one of the common metabolic disorders in Polycystic Ovary Syndrome (PCOS). Proprotein convertase subtilisin kexin type 9 (PCSK9) is a new component of lipid metabolism and correlated to the development of dyslipidemia and atherosclerosis. This protein acts by preventing the recycling of LDL receptors (LDL-r) back to the cell surface and thus generates higher levels of LDLc. The objective of this study was to evaluate the PCSK9 polymorphisms rs505151 (c.2009A>G), rs562556 (c.1420A>G) and rs11206510 (T>C) and plasma PCSK9 levels in PCOS. A group of women with PCOS (n=97), and a group of healthy women (control, n=99) were selected. Biochemical parameters were determined by using Vitros system and polymorphisms were assessed by TaqMan SNP Genotyping Assays. Plasma PCSK9 levels or PCSK9 polymorphisms were not associated with PCOS. The genotype rs11206510TT was associated with higher levels of PCSK9 in both groups. The population investigated (PCOS+control groups) with the rs505151AA genotype presented higher HDLc levels. The GG genotype regarding rs562556 polymorphism was associated with higher HDLc in PCOS group, while the AA genotype carriers had higher plasma testosterone levels when evaluated all women in a same group. The results were the same by comparing recessive and dominant model despite PCOS or both groups altogether. Our results suggest that PCSK9 is not altered specifically in PCOS, but it could be associated with in lipid and androgen metabolism in Brazilian women.


Asunto(s)
Predisposición Genética a la Enfermedad/genética , Síndrome del Ovario Poliquístico/genética , Polimorfismo de Nucleótido Simple/genética , Proproteína Convertasa 9/genética , Adulto , Brasil , Estudios de Casos y Controles , LDL-Colesterol/genética , Dislipidemias/genética , Femenino , Frecuencia de los Genes/genética , Genotipo , Humanos , Lípidos/genética , Receptores de LDL/genética
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