作者: Meng-Hsing Wu , Ming-Wei Lin
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摘要: Vitamin D plays a physiologic role in reproduction including ovarian follicular development and luteinization via altering anti-mullerian hormone (AMH) signalling, follicle-stimulating sensitivity progesterone production human granulosa cells1. It also affects glucose homeostasis through manifold roles. The potential influences of vitamin on include the presence specific receptor (VDR) pancreatic β-cells skeletal muscle, expression 1-α-hydroxylase enzyme which can catalyze conversion 25-hydroxy [25(OH)D] to 1,25-dihydroxyvitamin D, response element insulin gene promoter2. Polycystic ovary syndrome (PCOS) is common cause dysfunction women with anovulation. main symptoms are characterized by chronic anovulation, hyperandrogenism, and/or polycystic morphology from ultrasound examination. phenotypic manifestation this disorder associated various degrees gonadotropic metabolic abnormalities determined interaction multiple genetic environmental factors. prevalence deficiency PCOS about 67-85 per cent, serum concentrations 25(OH)D <20 ng/ml3. Although there no significant difference levels between normal control women, high has been found be may have great impact public health4. Low exacerbate PCOS, resistance, ovulatory, menstrual irregularities, infertility, obesity elevate risk cardiovascular diseases. Many observational studies suggest possible an inverse association status disturbances but it still hard draw definite conclusion causal relationship due inconsistent findings individual recent meta-analysis report systematic review5. Vitamin supplementation lower abnormally elevated AMH increase anti-inflammatory soluble for advanced glycation end-products D-deficient PCOS1. In particular, calcium addition metformin therapy could result beneficial effects regularity ovulation6. However, Garg et al7 recently demonstrated that was effect kinetics factors after at dose 4,000 IU/day six months, among treated metformin. Due small sample size relatively short duration follow up previous study clinical trial, relieving remain inconclusive6,7. Therefore, further research quality randomized controlled trials warranted establish management PCOS. Low significantly correlated resistance PCOS2. Thus, genes involved metabolism suggested as candidate susceptibility PCOS. A few polymorphisms VDR gene, such Cdx2, Taq1, Bsm1, Apa1, Fok1, were reported play influential secretion women8. Fok1 polymorphism protective type 2 diabetes mellitus, while Bsm1 had precipitating diabetes. Besides, Apa1 confer reduced deficiency8. In issue Dasgupta al9 present conducted Hyderabad city, India, investigate pattern four (Cdx2, Taq1) Indian women. They genotype allele frequency distributions Cdx2 higher heterozygous GA well observed controls when compared cases (P<0.001), indicating single nucleotide (SNP) against phenotype. After adjustment covariates age body mass index carriers conferring protecting other associations three (Fok1, examined genotypes some clinical/biochemical traits, testosterone showed infertility. Further, two haplotypes composed polymorphisms, ACCA ACTA, PCOS. In cohort Austrian levels10. others did not find differences frequencies controls4. We 1a promoter Taiwanese Asians women11. our subjects carrying 1521CG/1012GA haplotype both treatment only effective homozygous 1521G/1012A haplotype11. Despite several implicated results patients considerable disagreement and, therefore, these variants pathogenesis remains debatable. different ethnic origin or evolutionary force, drift selection pressure, even techniques genotyping assay. For example, variant substrate (IRS)-2 IRS-1 IRS-2 Chinese population Taiwan contradictory Caucasian African American populations12. When we minor populations11, opposite Caucasians Americans. This might partly explain populations. wide heterogeneity signs predisposed factors, easy evaluate putative functional correlations SNPs addition, many interlinking affect So far, inconclusive. Further investigations large independent cohorts diverse populations necessary clarify if ethnic-specific thresholds under interactions