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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 35  |  Issue : 2  |  Page : 463-469

Androgen receptor gene polymorphism and female sexual functionin Egyptian women


1 Department of Dermatology, Andrology and STDs, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Public Health & Community Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Department of Dermatology, Ministry of Health, Shebin AlKom General Hospital, Menoufia, Egypt
4 Department of Dermatology, Faculty of Medicine, Menoufia University, Menoufia, Egypt
5 Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Date of Submission11-Oct-2021
Date of Decision03-Nov-2021
Date of Acceptance07-Nov-2021
Date of Web Publication27-Jul-2022

Correspondence Address:
Sara E Elghazouly
Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_200_21

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  Abstract 


Background
Androgen receptor (AR) polymorphism in cytosine–adenine–guanine (CAG) repeat has an effect on the functional capacity of AR in males. However, little researches in this field are available regarding female sexual function.
Objectives
To investigate the possible link between polymorphism in CAG repeat of AR gene and female sexual function in a sample of Egyptian women.
Patients and methods
In all, 500 married Egyptian women completed a questionnaire regarding sociodemographic, reproductive, and sexual data. AR CAG repeat length was analyzed for those having female sexual dysfunctions using real-time PCR.
Results
The most sensitive domain to AR CAG repeat length was orgasm domain that showed significant positive correlations with short allele (P = 0.001), long allele (P = 0.015), biallelic mean (P = 0.000), and X-weighted biallelic mean (P = 0.000). Satisfaction domain had significant positive correlations with biallelic mean (P = 0.035) and X-weighted biallelic mean (P = 0.032). However, the pain domain was of significant negative correlations with AR polymorphism of short allele (P = 0.002), biallelic mean (P = 0.013), and X-weighted biallelic mean (P = 0.011).
Conclusions
AR polymorphism could represent a nonnegligible aspect in female sexual function. The lower AR CAG repeat polymorphism was of significant impact on female sexual dysfunction affecting mainly female orgasm, followed by pain disorders that finally reflected on her sexual satisfaction.

Keywords: androgen receptor, cytosine–adenine–guanine repeat polymorphism, female sexual function


How to cite this article:
Farag AG, Shehata YA, Elghazouly SE, Elshaib ME, Elhelbawy NG. Androgen receptor gene polymorphism and female sexual functionin Egyptian women. Menoufia Med J 2022;35:463-9

How to cite this URL:
Farag AG, Shehata YA, Elghazouly SE, Elshaib ME, Elhelbawy NG. Androgen receptor gene polymorphism and female sexual functionin Egyptian women. Menoufia Med J [serial online] 2022 [cited 2024 Mar 29];35:463-9. Available from: http://www.mmj.eg.net/text.asp?2022/35/2/463/352149




  Introduction Top


Female sexual dysfunction (FSD) is persistent and recurrent problems that occur during any phase of sexual response cycle and distress married women or strain their relationships with their partners. It may occur in all or in certain sexual situations[1]. As it is difficult to assess the degree of distress related to sexual symptoms in an extensive study[2] and the FSD parameters are not clear as in male sexual dysfunction, many difficulties were reported in the prevalence of FSD estimation[3]. In the sexual response cycle, there are four phases: excitement, then plateau, followed by orgasm, and finally resolution[3]. Disruption of any of its component results in sexual dysfunction that might be decreased sexual desire and/or disorders in sexual arousal, orgasm, and sexual pain[4]. In women, the role of testosterone is not quite clear. Testosterone may affect the female sexual function through its effect on cardiovascular, vaginal, and musculoskeletal health, and cognitive function. Testosterone therapy was revealed to have potentially optimistic effects on cardiovascular plus cognitive functions[5]. Circulating androgens might be inadequate to explain their action on the target tissues because these tissues may contribute to androgen production and/or its aromatization to estrogen, which act respectively through the androgen receptor (AR) and estrogen receptors[6]. AR is an essential element of the pathway of androgen signaling. It is found in many tissues that include the bone, muscle, brain, clitoris, and the vagina. When AR is activated (bind to testosterone or dihydrotestosterone), it is translocated from the cytoplasm to the nucleus[7]. The AR genetic code lies proximally on the long arm of the X-chromosome. The AR gene comprises eight exons. Cytosine–adenine–guanine (CAG) repeats were found on the first exon (eight to more than 30 repeats). These CAG repeats code for the polyglutamine sequence in the NH2-terminal domain of AR. By that way, these repeats determine the degree of AR transcriptional activity. The CAG sequence span correlates inversely with the sensitivity of AR to androgen and, consequently, with AR activity level[8]. In men, lower numbers of AR CAG repeats are related to a more transcriptional activity of AR that is expressed as a higher androgenic influence[9]. In opposition, a longer span in CAG repeats of AR is linked to a hypoandrogenic state and male infertility[10],[11]. In addition, polymorphism in CAG repeats of AR may affect the levels of circulating androgen[12]. Yet, the role of CAG repeat polymorphism in AR is blurred regarding woman sexual function[13]. Thus, the aim of this study was to investigate the possible link between the AR gene CAG repeat polymorphism and female sexual function in a sample of Egyptian women.


  Patients and methods Top


This is a cross-sectional study. It was conducted on 500 married Egyptian women during the period from December 2019 to June 2020. They were enrolled from the Gynecology and Obstetrics Clinic in Menoufia University, medical professionals, and employees working in that hospital as well as friends and colleges. We included sexually active married females. The exclusion criteria were females having (a) evident psychological disorders (e.g., depression and/or use of antipsychotic/antidepressant drugs in the previous 3 months), (b) neurological illnesses (e.g., multiple sclerosis and Parkinson), (c) a condition influencing sexual function and/or levels of sex hormones (e.g., pregnancy, lactation, and thyroid diseases). Ethical considerations: every member in the study was educated about the point of examination, its advantage to her, and to the network. An informed written consent was taken from each member before incorporating into the study. They reserve the option to decline without impact on their administration. All information acquired from members was utilized for logical purposes as it was. Researcher telephone number and all conceivable imparting techniques were provided to the members to return for any clarification.

Tools: each woman completed the standard questionnaire. Data were obtained regarding demographic data, which included age, occupation, educationl level, and bringing-up place, as well as socioeconomic level. Husbands' problems regarding desire and erection, and marital disorders were included. Reproductive data including circumcision, methods of contraception, years of marriage, having children, and previous marriage were addressed. Assessment of sexual disorder was done based on female sexual function index (FSFI)[14]. The Arabic translation of FSFI was utilized to assess FSD in which we evaluated six domains throughout the previous 4 weeks: (a) desire, (b) arousal, (c) lubrication, (d) orgasm, (e) satisfaction, and (f) pain. Score less than 65% of each domain represent sexual dysfunction in this domain. The total score was calculated by summation of the all domain scores. It had a range from 2.0 to 36.0. Total score less than or equal to 23 means sexual dysfunction (the patient group), and more than 23 means normal sexual function (the control group)[15].

Laboratory investigations: for females having FSD, 5 ml of blood was collected under aseptic situation in an EDTA tube for DNA extraction. Genomic DNA was extracted and purified from whole blood utilizing QIAamp DNA Mini Kit (Qiagen, Düsseldorf, Germany; 2012) [email protected] according to the manufacturer's protocol. Purified DNA was quantified using the NanoDrop spectrophotometer and stored at −20 till analysis. We determined the number of CAG repeats in each woman by four different measures[16]: (a) The number of CAG repeats in the allele containing the fewest CAG repeats (short allele). (b) The number of CAG repeats in the allele containing the most CAG repeats (long allele). (c) The mean number of CAG repeats of the long and short allele (calculated biallelic mean). (d) The number of CAG repeats in the active X-chromosome based on X-inactivation analysis (X-weighted biallelic mean). Extracted DNA was divided into two aliquots, one was mixed with 10 U of an HpaII restriction enzyme (Roche Diagnostic Systems, Mannheim, Germany), and the other was mixed with a buffer containing no enzyme. Samples were incubated overnight at 37°C, followed by a final enzyme denaturation step at 95°C for 5 min; by this step, the non-methylated (active X) DNA segments were digested by the enzyme and are thereby unavailable for PCR amplification, while the methylated (inactive X) segments were not digested by the enzyme and remain intact for amplification[17]. The digested and undigested samples were recorded and used for the following PCR reaction for the amplification of short and long allele of the CAG repeat region in the first exon of the AR gene on the X-chromosome. The following published primers flanking the CAG repeats were used for amplification: primers for short allele (allele 1), forward primer 5′-TCCAGAATCTGTTCCAGAGCGTGC-3′, reverse primer 5′ GCTGTGAAGGTTGCTGT TCCTCAT-3′ and primers for long allele (allele 2), forward primer 5′-CTGGA GAACCCGCTGGACTA-3′, and reverse primer 5′-GCCCATTTCGCTTTTGACA-3′. The genomic DNA of digested and undigested samples was applied as a template for real-time PCR using SYBR Green II with low ROX (QuantiTect SYBR Green PCR Kit; Applied Biosystems, Waltham, Massachusetts, USA) in an Applied Biosystems 7500, software version 2.0.1 (Applied Biosystems). The running program was as follows: 94°C for 5 min, followed by 35 cycles of denaturation at 94°C for 30 s, annealing at 56.4°C for 30 s, and extension at 72°C for 30 s. All samples were analyzed in duplicate in nondigested and digested conditions. For calculations of allele inactivation, the variables were signal allele 1 digested (a), signal allele 2 digested (b), signal allele 1 undigested (c), and signal allele 2 undigested (d). In calculating the degree of X-inactivation for individuals, we used the average value of the duplicate samples for both digested and undigested DNA samples in the calculations. To compensate for unequal amplification of alleles due to confounding factors not caused by methylation, signals c and d (undigested samples) are necessary to create a correction factor: inactivation of allele 1 (a/c)/(a/c b/d) (equation I) and inactivation of allele 2 (b/d)/(a/c b/d) (equation II). For determination, the mean number of CAG repeats of the active allele (X-weighted biallelic mean), each allele length was multiplied by its total contribution to expression (1 minus the methylation status), and each adjusted weight allelic mean value was added together to obtain the overall X-weighted biallelic mean for each woman.

Statistical analysis

The collected data was tabulated and then analyzed using an IBM personal computer with the Statistical Package of the Social Sciences (SPSS), version 20 (SPSS; IBM Corp., Armonk, New York, USA). Descriptive and analytical statistics included χ2 test and Student's t test. Odds ratio (OR) was also included. P value less than 0.05 was characterized to be statistically significant.


  Results Top


Sociodemographic characteristics

The studied females' age ranged from 17 to 65 years. More than half of the studied females were from urban areas (283/500, 56.8%). Most of our participants were highly educated (361/500, 72.2%) and had moderate socioeconomic level (327/500, 65.4%). About half (49%) of the studied females had professional work. Most of the participants were circumcised (321/500, 64.2%) and not previously married (485/500, 97%), and their marriage period ranged from 1 to 30 years. Among the participants, 477 (95.4%) females had children with the mean of two children. About half (46.6%) of the studied females were intrauterine device users [Table 1].
Table 1: Sociodemographic features of the studied individuals

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Female sexual dysfunctions prevalence and its risk factors

Based on the analysis of FSFI recorded data, FSD was reported in 100 females. Therefore, the FSD prevalence was 25% of our participants. Older females (P < 0.001), rural residency (P = 0.009), lower education (P < 0.001), not working/no professional job (P < 0.001), lower socioeconomic class (P < 0.001), circumcision, Oral contraceptive (OCP), presence of bad marital relation, and Erectile dysfunction (ED) were significantly found to be potential risk factors for FSD [Table 1].

Female sexual function index domains among the studied females

The arousal (P < 0.001), orgasm (P < 0.001), lubrication (P < 0.001), and satisfaction (P < 0.001) domains showed significant lower mean values in the FSD group than normal. However, desire and pain domains showed nonsignificant difference (P = 0.106 and 0.913, respectively) [Table 2].
Table 2: Difference between normal participants and the female sexual dysfunctions group as regards each domain score of female sexual function index

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Multiple logistic regression analysis technique to determine the effect of potential risk factors on FSD showed that low education was the highest risk factor affecting FSD (P = 0.001; OR = 12.872) increasing the risk of FSD by 13 times, followed by low male desire (P = 0.001; OR = 7.722) and presence of circumcision (P = 0.01; OR = 4.771), which increase the FSD risk by about eight and five times, respectively. On the other hand, male erection was the lowest risk factor affecting FSD (P = 0.049, OR = 1.030) [Table 3].
Table 3: Determination of the effect of potential risk factors on female sexual dysfunction using multiple logistic regression analysis technique

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Relationships between AR CAG repeat polymorphism and different FSFI domain disorders (n = 100).

The most sensitive domain to AR CAG repeat polymorphism changes was the orgasm domain, followed by pain, and then satisfaction domain. There were significant positive correlations between orgasm domain mean value and AR CAG repeat polymorphism of short allele (r = 0.322, P = 0.001), long allele (r = 0.243, P=0.015), biallelic mean (r = 0.353, P < 0.001), and X-weighted biallelic mean (r = 0.363, P < 0.001). Regarding satisfaction domain, it had significant positive correlations with mean value and AR CAG repeat polymorphism of biallelic mean (r = 0.211, P = 0.035) and X-weighted biallelic mean (r = 0.215, P = 0.032). On the other hand, there were significant negative correlations between pain domain and AR CAG repeat polymorphism of short allele (r=−0.299, P = 0.002), biallelic mean (r=−0.248, P = 0.013), and X-weighted biallelic mean (r=−0.253, P = 0.011) [Table 4], [Figure 1] and [Figure 2].
Figure 1: Amplification plot of CAG gene [normalized fluorescence signal (ΔRn) plotted versus cycle number]. CAG, cytosine–adenine–guanine.

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Figure 2: Mean of CAG repeats in androgen receptor alleles. CAG, cytosine–adenine–guanine.

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Table 4: Relationships between androgen receptor cytosine-adenine-guanine repeat polymorphism and different female sexual function index domain disorders

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  Discussion Top


Studying the AR CAG tri-repeat polymorphism revealed that long CAG repeats were associated with decreased AR sensitivity[9] and sexual pain[8],[10]. However, Wåhlin-Jacobsen et al.[16] reported that longer CAG repeats were linked to better sexual function in females. Therefore, we hypothesized that analyzing AR CAG tri-repeat polymorphism could add to our understanding regarding the biological aspects of female sexual function.

The results of the current study point to the impact of AR CAG repeat polymorphism on female sexual function, reporting that the decreasing numbers of CAG repeats have been linked to improper and decreased sexual function specially toward orgasmic problems. However this result was against our expectation, as shorter AR CAG repeat polymorphisms had a link with increased AR transcriptional activity[9], and with elevated androgen levels, and longer CAG repeats in AR gene were related to hypoandrogenicity[11]. A potential explanation for our finding could be the shape of the AR CAG repeat length versus the receptor function curve. This curve may be a bell-shaped curve, with one or more pits having low functional amplitude at each end, or the curve might have a shape of a staircase. In addition, the CAG repeats of the number did not significantly impact the AR sensitivity to testosterone in women, as reported in men[18]. Moreover, androgen serum levels have a nonsignificant effect on sexual function in females[8]. Furthermore, the women's sexuality, biopsychosocial nature, and their sexual function make it hard to detect reliable relationships in small trials or to identify the impact of a solitary factor on sexuality[16].

In this study, sexual function was assessed for all studied females using the Arabic translation of FSFI. By this standardized questionnaire, we observed FSD in 25% of females. This relatively low prevalence of FSD could be attributed to cultures in our locality as women who believed having sexual problems admitted that they did not seek medical help. They said that 'This is an embarrassing topic.'

Regarding FSFI domains, as previously reported[19], we found that the arousal, lubrication, and orgasm as well as satisfaction domains were significantly lower in FSD cases than normal ones.

In the current study, CAG repeat of long allele showed the highest mean value (33.66). However, the mean values for CAG repeat of short allele, biallelic mean, and X-weighted biallelic mean were 23.71, 28.41, and 14.04, respectively. However, Wåhlin-Jacobsen et al.[16] studied 529 Danish females. They found that the mean length of CAG repeats were 23.2 for the long allele, 20.3 regarding the short allele, and 21.7 for the biallelic mean, plus 21.7 for the mean of X-weighted biallelic[20]. The AR gene CAG repeat polymorphism in postmenopausal Brazilian females is also studied. They reported that the CAG repeat numbers had a range from 15 to 30. The difference between our result and that described by others[17],[20] could be explained by ethnic and interethnic variations in the CAG repeat polymorphism and/or allele fixation methods[21].

The women's ability to have orgasm is realized as an entirely developed skill, which depends on the social and cultural conditioning; nevertheless, orgasmic dysfunction was inherited in about one-third of cases highlighting the effect of biological issues in the feminine sexual function[22].

In the existing study, the most sensitive domain to AR CAG repeat polymorphism changes was orgasm that showed significant positive correlations with CAG repeats in AR polymorphism of long allele, short allele, biallelic mean plus X-weighted biallelic mean. This means that a tendency to decreased length in CAG repeat is linked to orgasmic dysfunction. Confirming this result, Wåhlin-Jacobsen et al.[16] found that females having problems in reaching orgasm had a significantly lesser CAG repeat span than females reporting no orgasmic difficulties.

In spite of the ongoing argument on the basis of female orgasms, sufficient clitoral stimulation might be essential for females to achieve orgasm. In addition genital arousal in women is associated with increased genital tissue blood flow, especially to the clitoris that is regulated by the vascular smooth muscle tone of the clitoral erectile tissue[22]. Different neuropeptides and neurotransmitters are involved in this process. In addition, androgens are supposed to adjust the synthesis and secretion as well as reuptake of those neurotransmitters[23].

On the basis of the aforementioned data, we might suggest that AR CAG repeat polymorphisms may affect AR function that could participate in the ability of females to achieve orgasm through androgen special effects on genital erectile tissues.

It was hypothesized that longer AR CAG repeats are linked to FSD in those primarily complaining of sexual pain[16],[24]. Recently, the Sutter et al.[8] study significantly demonstrated an inverse correlation between CAG repeat span length and presence of dyspareunia. In agreement with this hypothesis, we reported a significant link between pain disorder and increased CAG repeats in short, biallelic, and X-weighted biallelic means. Consequently, higher numbers of AR CAG repeats were linked to more frequent and/or more severe sexual pain, which might negatively affect the sexual relationship.

It was reported that sex hormones affect the perception of pain as estrogen and androgen receptors are identified in both central and peripheral nervous systems[25]. Sex steroids could modify neurotransmission in the brain and spinal cord as well as peripheral nerves, and alter their excitability by influencing the accessibility of their own receptors and other ligands including serotonin and opiates. In addition, peripheral tissues (away from the nervous and reproductive system) are affected also by steroid hormones; therefore, alterations in their structure and/or function secondary to variations in the level of sex steroids could disrupt pain sensation[26]. In the same content, we reported significant positive correlations between FSFI satisfaction domain with CAG biallelic and X-weighted biallelic mean. This means that the decreased CAG repeat is associated with improper and lower sexual satisfaction. This result was in settlement with that of Wåhlin-Jacobsen et al.[16]. The authors reported a significant decrease in mean CAG repeats of short allele and FSFI satisfaction disorder, and a presence of longer CAG repeat lengths were connected to good sexual function. In line with Wåhlin-Jacobsen et al.[16], we observed a nonsignificant relationship between low female sexual desire and AR CAG repeat length, indicating that the CAG repeat lengths did not impact sexual desire in women. Supporting this result, Elaut et al.[27] reported that female sexual desire was increased in women with both short and long AR CAG repeats. However, evaluation of AR CAG repeat lengths is not a portion of routine laboratory workup during the assessment of FSD or in any further endocrine condition such as idiopathic hyperandrogenism[28]. It could help in understanding the pathophysiological processes behind FSD[29].


  Conclusions Top


The AR CAG repeat polymorphism could represent a nonnegligible issue in women sexual function. The lower AR CAG repeat span was of significant impact on FSD affecting mainly female orgasm, followed by pain disorders that finally reflected on her sexual satisfaction.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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