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. 2021 Jun 30;18(13):7006.
doi: 10.3390/ijerph18137006.

Association between GnRH Receptor Polymorphisms and Luteinizing Hormone Levels for Low Ovarian Reserve Infertile Women

Shun-Long Weng  1   2   3 , Shu-Ling Tzeng  4   5 , Chun-I Lee  6   7   8 , Chung-Hsien Liu  6   7 , Chun-Chia Huang  8 , Shun-Fa Yang  4   5 , Maw-Sheng Lee  4   6   8 , Tsung-Hsien Lee  4   6   8
Affiliations

Association between GnRH Receptor Polymorphisms and Luteinizing Hormone Levels for Low Ovarian Reserve Infertile Women

Shun-Long Weng et al. Int J Environ Res Public Health. .

Abstract

The choice of ovarian stimulation protocols in assisted reproduction technology (ART) cycles for low ovarian reserve patients is challenging. Our previous report indicated that the gonadotrophin-releasing (GnRH) agonist (GnRHa) protocol is better than the GnRH antagonist (GnRHant) protocol for young age poor responders. Here, we recruited 269 patients with anti-Müllerian hormone (AMH) < 1.2 ng/mL undergoing their first ART cycles for this nested case-control study. We investigated the genetic variants of the relevant genes, including follicular stimulating hormone receptor (FSHR; rs6166), AMH (rs10407022), GnRH (rs6185), and GnRH receptor (GnRHR; rs3756159) in patients <35 years (n = 86) and patients ≥35 years of age (n = 183). Only the genotype of GnRHR (rs3756159) is distributed differently in young (CC 39.5%, CT/TT 60.5%) versus advanced (CC 24.0%, CT/TT 76.0%) age groups (recessive model, p = 0.0091). Furthermore, the baseline luteinizing hormone (LH) levels (3.60 (2.45 to 5.40) vs. 4.40 (2.91 to 6.48)) are different between CC and CT/TT genotype of GnRHR (rs3756159). In conclusion, the genetic variants of GnRHR (rs3756159) could modulate the release of LH in the pituitary gland and might then affect the outcome of ovarian stimulation by GnRHant or GnRHa protocols for patients with low AMH levels.

Keywords: GnRH agonist; GnRH antagonist; GnRH receptor; POSEIDON criteria; anti-Müllerian hormone; assisted reproduction technology; poor responders; single nucleotide polymorphism.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Representative TaqMan assay for AMH rs10407022 genotyping. The FAM (blue) and VIC (green) fluorescence probes detect T and G alleles, respectively. The ROX (red) fluorescence probes are used for calibration.
Figure 2
Figure 2
Representative TaqMan assay for FSHR (rs6166) genotyping. The FAM (blue) and VIC (green) fluorescence probes detect A and G alleles, respectively. The ROX (red) fluorescence probes is used for calibration.
Figure 3
Figure 3
Representative TaqMan assay for GNRH1 (rs6185) genotyping. The FAM (blue) and VIC (green) fluorescence probes detect G and C alleles, respectively. The ROX (red) fluorescence probes is used for calibration.
Figure 4
Figure 4
Representative TaqMan assay for GnRHR (rs3756159) genotyping. The FAM (blue) and VIC (green) fluorescence probes detect C and T alleles, respectively. The ROX (red) fluorescence probes is used for calibration.
Figure 5
Figure 5
The baseline LH levels for patients with various GnRHR rs3756159 genotypes. There was no significant difference of these LH levels between CC vs. CT/TT genotypes in young (POSEIDON group 3, p = 0.095) or advanced age (POSEIDON group 4, p = 0.152) patients by Mann–Whitney U test.
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