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Plymorphism of CYP17 for Polycystic Ovarian Syndrome in Women of Salah Al-Din Provence/ Iraq
Author(s) -
Hadeel Abdulhadi Omear,
Adil F. Shehab,
Akeel Al-Assie
Publication year - 2014
Publication title -
maǧallaẗ markaz buḥūṯ al-taqniyyaẗ al-aḥyāʾiyyaẗ
Language(s) - English
Resource type - Journals
eISSN - 2708-1370
pISSN - 1815-1140
DOI - 10.24126/jobrc.2014.8.1.305
Subject(s) - testosterone (patch) , genotype , endocrinology , hormone , medicine , allele , prolactin , polycystic ovary , body mass index , allele frequency , biology , gene , sex hormone binding globulin , physiology , obesity , genetics , androgen , insulin resistance
CYP17 gene is the key in the metabolic pathway of sexual steroids, it codes for two enzymes 17–alpha hydroxylase and 17, 20 lyase who play an important role in the production of sex steroid hormones. The current study included study of the relationship of this gene with PCOS women in reproductive age. Blood samples were collected from two groups of women: first group consists of 98 women infected with polycystic ovaries syndrome, the second consists of 25 healthy women to detect the presence of mutation within the gene, then calculate allele frequency of mutant and wild allele for this gene, then repeat genotypes in infected women and compared with healthy once, were calculated body mass index BMI of two groups and measure the level of sex hormones (LH, FSH, Prolactin, Testosterone) in both groups, were the results showed significant differences between patients and healthy women in BMI and the level of hormones (LH, Prolactine) while there is no significant differences in the (FSH, Testosterone) hormone. Three pattern of genotype were obtained: TT, homozygous wild, (TC) much lower than the frequency in the healthy 0.82 while the frequency of allele C among patients 0.44, which is more than double than in healthy 0.18. The current results showed absence CC genotype in healthy women and appeared only in women with PCOS. This monitor the presence of link between this gene and PCOS as may be considered the mutation -34 (T C) in the promoter of gene CYP17 marker of the disease.

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