چكيده لاتين :
Background: Polycystic ovary synd rome (PCaS) is related to obes ity and to major metabolic
alterations including both insulin resistance and beta-cell dysfunction. Ghrelin was identified as the
endogenous ligand for the growth hormone secretagogue (GHS) receptor. The actio ns of ghre lin are
carried out through interaction with specific receptor, named GHS-R.
Objective: In a case-control study, we compared the expression of ghrelin and GHS-Rs mRNA by
Quantitative Real-time PCR method in studied groups in order to determine the role of ghrelin and
GHS-Rs in pathogenesis of PCas.
Materials & Methods: Follicular fluid samples were obtained at oocyte collection from 22 pat ients
undergoing IVF-ET as control and 11 patients were diagnosed as having pcas. Tota l RNA was
extracted from isolated follicular fluid cells and Zug RNA was diluted and reverses transcribed
using random primers and Superscript II. Specific primers for the ghrel in, GHS-R Ia and GHS-R Ib
were designed. Sample were run in triplicate on an AB! Geneamp 5700 sequence detection system.
They were subjected to 40 cycle s of amplification under conditi on 92°C- 20s and 62°C-I min using
3 ~t1 diluted eDNA (1 :7), 1O ~ 1 2X SYBR green, 3~1 diluted eDNA. p-actin mRNA was assayed and
then normalized to total RNA measurements for each sample.
Resu lts: Age, weight and resulting pregnancies did not vary between pcas and non-peaS
patients, whereas the BMI and serum testosterone level of pcas were significantly higher than
non-Pf.OS patients. Quantitative real-time RT-PCR showed that mRNA for ghrelin and GH -R Ib
were detectab le in follicular fluid cells from all patients. We failed to tind mRNA for GHS-R Ia in
any of foll icular fluid cells. There were no significant difference in ghrelin and GHS-R Ib mRNA
expression levels between pcas and non-PfיOיS groups.
Conclusion: Our findings indicate that ghrelin and ghrelin receptors may not be cons idered risk
factors for pathogenesis of pc a s .
