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. 2022 Oct 13;15(1):111.
doi: 10.1186/s13048-022-01047-4.

Anti-Müllerian hormone independently affect mtDNA copy number in human granulosa cells

Affiliations

Anti-Müllerian hormone independently affect mtDNA copy number in human granulosa cells

Anom Bowolaksono et al. J Ovarian Res. .

Abstract

Background: Recently, as a delayed childbearing trend is emerging in modern women's adulthood, diminished reproductive potential due to age-related changes is more prevalent. Reduction in the abundance of mitochondrial DNA (mtDNA) copies and circulating anti-Müllerian hormone (AMH) have been separately reported with aging, contributing to the decrease in successful reproduction. However, there are limited reports on the impact of age on mtDNA and AMH in the same individual and whether mtDNA copy numbers are influenced by age and AMH.

Methods: In the present study, we utilized a real-time quantitative PCR (RT-qPCR) to quantify the mtDNA copy number of granulosa cells obtained from 43 women undergoing an in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI) program.

Results: According to our analysis, a significant correlation was observed between age and mtDNA copy number (r = -0.54, P < 0.001) and between age and AMH level (r = -0.48, P < 0.001) of the same individual. There was also a positive correlation between mtDNA copy number and AMH (r = 0.88, P < 0.001) with AMH level falling as mtDNA decreases. In our regression, age and AMH were shown to have low collinearity (VIF = 1.297) but only AMH was correlated with mtDNA quantity (P < 0.001).

Conclusion: Our study suggests that both mtDNA and AMH abundance are influenced by age and that AMH levels independently affect mtDNA copy number regardless of age. Further research is required to understand the role of AMH on mitochondria bioenergetics.

Keywords: Aging; Anti-Müllerian hormone; Fertility; Granulosa cells; Mitochondrial DNA (mtDNA).

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Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Fig. 1
Fig. 1
Comparison of mitochondrial DNA (mtDNA) copy number between normal weight (NW) [N = 24], overweight (OW) [N = 14], and obese (OB) [N = 5] subjects (A), between LH-administered [N = 27] and non-administered subjects [N = 16] (B), and between GH-administered [N = 22] and non-administered subjects [N = 21] (C). mtDNA copies are relatively quantified to the amount of B2M. All values are expressed as mean ± standard deviation (SD) obtained from two separate experiments (Duplo). (BMI group was analyzed by ANOVA; LH and GH group were analyzed by t-test). *ns: not significant
Fig. 2
Fig. 2
Simple linear regression between age and mtDNA copy number (r = −0.54, P < 0.001) (A), between age and AMH level level (r = −0.48, P < 0.001) (B), and between AMH level and mtDNA copy number (r = 0.88, P < 0.001) (C). mtDNA copies are relatively quantified to the amount of B2M. All values are expressed as mean ± standard deviation (SD) obtained from two separate experiments (Duplo) (Data was analyzed using Pearson’s correlation)
Fig. 3
Fig. 3
Comparison of pregnancy frequency according to age (A), mtDNA copy number (B), and age (C) when stratified into < 35 and ≥ 35 years old. mtDNA copies are relatively quantified to the amount of B2M. All values are expressed as mean ± standard deviation (SD) obtained from two separate experiments (Duplo) (Pregnancy data according to mtDNA copies and age were analyzed using a t-test; pregnancy proportion according to age group was analyzed using Fisher’s exact test). *ns: not significant

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