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The Journal of Clinical Endocrinology & Metabolism Vol. 92, No. 5 1871-1874
Copyright © 2007 by The Endocrine Society

Serum Anti-Mullerian Hormone Concentrations Are Not Altered by Acute Administration of Follicle Stimulating Hormone in Polycystic Ovary Syndrome and Normal Women

Deborah S. Wachs, Mickey S. Coffler, Pamela J. Malcom and R. Jeffrey Chang

Department of Reproductive Medicine, University of California, San Diego, La Jolla, California 92093

Address all correspondence and requests for reprints to: R. Jeffrey Chang, M.D., Department of Reproductive Medicine, University of California, San Diego, School of Medicine, 9500 Gilman Drive, La Jolla, California 92093-0633. E-mail: rjchang{at}ucsd.edu.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Context: In the human ovary, expression of anti-Mullerian hormone (AMH) is detected primarily in granulosa cells of preantral and small antral follicles. This finding is consistent with the tight correlation between circulating AMH levels and the number of small antral follicles (2–5 mm) in normal and polycystic ovary syndrome (PCOS) women. In addition, the greater follicle count in PCOS is mirrored by significantly higher serum AMH levels compared with those of normal women. Despite the utility of AMH measurements in evaluating ovarian physiology and function, the regulation of AMH remains poorly understood.

Objective: The objective was to determine whether gonadotropins acutely regulate serum AMH in women with PCOS and normal women.

Design: We conducted a prospective study to compare ovarian responses to FSH in two groups of women.

Setting: The study was conducted in a General Clinical Research Center in a tertiary academic medical center.

Patients: Women with PCOS (age, 18–35 yr; n = 16) and normal ovulatory controls (age, 18–35 yr; n = 11) were recruited for study.

Interventions: Serum samples were measured over a 24-h period after an iv injection of recombinant human FSH (150 IU).

Main Outcome Measure(s): Serum AMH responses after FSH administration were measured.

Results: Basal serum AMH levels were markedly increased in women with PCOS compared with levels observed in normal women. After FSH injection, PCOS women failed to demonstrate changes in circulating AMH over 24 h. A similar lack of alteration in serum AMH was observed in normal women.

Conclusions: These findings suggest that in PCOS and normal women, acute exposure to FSH does not appear to exert an effect on AMH production.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
IN THE PROGRESSION of human ovarian follicle growth, anti-Mullerian hormone (AMH) mRNA expression is initially detected in granulosa cells of primary follicles. With subsequent development, the concentration of AMH intensifies to achieve the greatest expression in large preantral and small antral follicles (1, 2, 3). Thereafter, the expression declines and is not observed in late stage antral follicles, preovulatory follicles, or the corpus luteum. The precise role of AMH in ovarian physiology is not completely understood, although two potential functions have been proposed. First, it has been reported that AMH may serve to inhibit recruitment of primordial follicles into the pool of growing follicles to prevent early depletion (3, 4). Second, AMH may decrease follicle sensitivity to gonadotropin stimulation to control the number of large preantral and small antral follicles that reach the preovulatory stage (4, 5). These proposed actions of AMH are consistent with the report of decreased AMH expression in preantral and early antral follicles of women with PCOS compared with values observed in normal women (6). In addition, the number of small antral follicles in PCOS women and normal women has been positively correlated to circulating levels of AMH. With two functions so critical to folliculogenesis, the regulation of AMH is paramount in understanding its role. However, the regulation of AMH production by granulosa cells is not well understood.

To explore the role of FSH on granulosa cell production of AMH, basal and 24-h patterns of AMH secretion were studied after acute FSH stimulation in women with PCOS and normal women.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

Sixteen women with PCOS (ages 18–35 yr) and 11 normal women with regular menstrual cycles (ages 18–35 yr) were recruited for study. All PCOS subjects exhibited clinical and biochemical evidence of hyperandrogenism and were either oligomenorrheic or amenorrheic. In PCOS and normal control groups, the mean (±SE) ages were 26.3 ± 1.3 and 28.8 ± 1.7 yr, respectively, and not significantly different. The mean body mass index was significantly greater in the PCOS subjects compared with that of the normal controls (34.9 ± 1.9 vs. 28.6 ± 1.5 kg/m2, respectively; P < 0.05). Each PCOS subject exhibited ultrasound evidence of bilaterally enlarged polycystic ovaries. Late-onset congenital adrenal hyperplasia was excluded by a serum 17-hydroxyprogesterone (17-OHP) level of less than 3 ng/ml. Circulating TSH and prolactin levels were normal and not significantly different between groups. The normal subjects were monitored by menstrual calendar for 3 months and by urinary LH testing for 1 month before study to establish the regularity of their cycles. None of the subjects in either group had received any hormone medication for at least 3 months before study. The study had been approved by the Institutional Review Board at the University of California, San Diego, and written informed consent was obtained from each participant before study.

Methods

Each subject was admitted to the General Clinical Research Center at the University of California, San Diego, on the day of testing. In normal subjects, testing was performed during the midfollicular phase defined as d 5–8. After baseline sampling, recombinant human FSH (r-hFSH) was administered as an iv bolus at a dose of 150 IU. The r-hFSH (Gonal-F) was kindly provided by Serono Laboratories, Inc. (Rockland, MA). None of the PCOS subjects had experienced recent ovulation, as evidenced by serum progesterone (P4) levels of less than 1 ng/ml at the baseline sample. Blood samples were drawn through an indwelling iv catheter at 1-h intervals for 2 h before and at 1, 2, 3, 4, 6, 8, 10, 12, 16, 20, and 24 h after r-hFSH administration. Samples were allowed to clot, and sera were separated by centrifugation and stored at –20 C until assayed. Individual serum samples were analyzed in the same assay in duplicate.

Assays

Serum concentrations of LH and FSH were measured by RIA with intra- and interassay coefficients of variation (CV) of 5.4 and 8.0%, respectively, for LH and 3.0 and 4.6%, respectively, for FSH (Diagnostic Products Corp., Los Angeles, CA). Serum concentrations of estrone (E1), estradiol (E2), androstenedione (A), and testosterone (T) were measured by well-established RIA with intraassay CV less than 7%. P4, 17-OHP, and dehydroepiandrosterone sulfate (DHEAS) were measured by RIA with intraassay CV less than 7% (Diagnostic Systems Laboratories, Inc., Webster, TX). SHBG was determined by the Diagnostic Systems Laboratories 6300 kit with intra- and interassay CVs, 2.5 and 3.73%, respectively. Serum concentrations of AMH were measured by ELISA with intra- and interassay CV of 4.12 and 6.19%, respectively (Diagnostic Systems Laboratories, Inc.).

Statistical analysis

Baseline hormone values between PCOS and normal women were compared by group t tests using SPSS software (SPSS, Inc., Chicago, IL). Where applicable, significance testing was two-sided at a 5% significance level.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Baseline studies

Baseline hormone values are shown in Table 1Go. In PCOS women, mean (±SE) circulating levels of LH, A, T, and E1 were significantly greater than those of normal controls. By comparison, the mean SHBG level was significantly lower than that of normal women. Basal levels of serum FSH, DHEAS, 17-OHP, E2, and P4 were similar in both groups.


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  		TABLE 1. Mean endocrine-metabolic values (±SE) of PCOS and normal women

 
Serum FSH and E2 levels after r-hFSH administration

Intravenous administration of r-hFSH, 150 IU, resulted in a rise in circulating FSH levels in PCOS and normal women within 1 h of injection (Fig. 1Go). Subsequently, there was a gradual decline with a return to baseline values by 24 h. Corresponding increases in circulating E2 were observed in PCOS and normal women after r-hFSH, although maximal levels achieved in PCOS subjects were significantly greater than that observed in the normal control group (Fig. 1Go).


Figure 1
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  		FIG. 1. Mean (±SE) serum AMH levels after administration of r-hFSH (150 IU) in PCOS and normal women.

 
Serum AMH levels before and after r-hFSH administration

Basal levels of serum AMH in PCOS women were 3.4-fold higher than those of normal women (P < 0.001), which is consistent with previously published reports (7, 8, 9, 10, 11, 12, 13). In women with PCOS, administration of r-hFSH failed to induce any significant change in circulating concentrations of AMH because values remained constant over 24 h (Fig. 2Go). A similar pattern of response was observed after r-hFSH, although the magnitude of AMH secretion was considerably less than that of PCOS women (Table 2Go).


Figure 2
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  		FIG. 2. Mean (±SE) serum FSH and E2 concentrations after administration of r-hFSH (150 IU) at t = 0 in PCOS and normal women.

 

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  		TABLE 2. Baseline, mean maximal, and fold-change (±SE) serum AMH responses to r-hFSH (150 IU) in PCOS and normal women

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The results of this study have demonstrated that in PCOS women, elevated levels of circulating AMH were unchanged over a 24-h period after administration of FSH. In normal women, a similar lack of AMH response to FSH was also observed, although the magnitude of AMH secretion was considerably less. These findings suggest that in PCOS and normal women, acute exposure to FSH does not appear to exert an effect on AMH production.

We have previously employed iv FSH stimulation to determine the capacity of granulosa cells to produce E2 in PCOS and normal women (14). Using this experimental paradigm in the current study, circulating concentrations of FSH rose abruptly after injection to achieve peak levels within minutes of administration. Subsequent increases in serum E2 were observed in both groups, although the magnitude of response was greater in women with PCOS compared with that of normal controls. Therefore, the failure to observe increases in serum AMH after FSH was not due to inadequate provocative stimulation.

The failure of FSH to acutely alter serum AMH in women is not consistent with previous in vitro studies that have demonstrated an inhibitory effect of FSH on AMH mRNA expression and production in ovarian follicle cells. In immature rats pretreated with a GnRH antagonist, daily FSH was associated with an inhibition of AMH mRNA in granulosa cells of preantral and small antral follicles (2). Interestingly, when estradiol benzoate was administered either alone or in combination with FSH in these animals, AMH expression was similarly inhibited, suggesting that estrogen may also interfere with AMH production. Recent in vitro studies have demonstrated that short-term incubation of PCOS granulosa cells with FSH significantly reduced AMH production compared with a lack of response in granulosa cells obtained from normal ovaries (15). Based on these in vitro results, a decrease in serum AMH after FSH might have been expected in PCOS and normal women rather than an unaltered AMH response. However, the in vivo regulation of AMH in women may be different compared with rodents and involve more complex interactions than those observed in isolated granulosa cell culture systems. For instance, despite elevated basal levels of AMH in PCOS women, there has been no evidence of AMH-induced aromatase inhibition as reported in studies of fetal ovaries of rats and sheep (16, 17). In addition, we have previously shown that in women with PCOS, administration of a similar dose of FSH stimulated a distinctive increase of serum E2 that occurred 2 h after injection and achieved maximal concentrations by 10 h that were well above those observed for normal women (14). These findings may reflect the marked stimulatory effect of FSH on aromatase activity compared with a relatively lesser influence by AMH. It is noteworthy that inhibition of aromatase production by cultured fetal ovaries treated with AMH required a relatively long period of exposure, 3 d, to achieve maximal effect (16). This delay suggested that AMH acted to disrupt enzyme biosynthesis rather than a direct effect on enzyme activity.

An effect of increased circulating FSH induced by iv injection together with the accompanying heightened E2 response had little influence on serum AMH levels. Alternatively, in PCOS women any suppression of granulosa cell AMH production by FSH and E2 may have been offset by a stimulatory effect of LH because cultured PCOS granulosa cells incubated with LH have been observed to produce significant increases in AMH compared with normal granulosa cells similarly treated (18).

Our findings are compatible with recent reports that have shown an unaltered pattern of AMH production throughout the normal menstrual cycle, including the early follicular and midcycle phases during which increases of FSH occur (19, 20). In addition, our results are not necessarily inconsistent with serum AMH responses to gonadotropin administration during ovulation induction in women undergoing controlled ovarian hyperstimulation (COH) (12, 21, 22, 23). In these studies, continuous administration of FSH in both normal and PCOS women resulted in an eventual decline of circulating AMH levels before human chorionic gonadotropin injection to trigger ovulation. Interestingly, in each study, commencement of FSH stimulation was not associated with an early change of serum AMH, which is equivalent to AMH responses to FSH in the current study. In response to standard doses of FSH, the AMH decrement was observed as early as 2 d, whereas with a low-dose protocol a significant decrease was apparent only after about 7–10 d (22, 23). In one study it was suggested that the delayed decrease of AMH after FSH may have reflected a threshold FSH dose below which an alteration in AMH is not observed (22).

In consideration of the relatively delayed decrease in serum AMH after FSH administration during COH, AMH responses may not have resulted from a direct result of gonadotropin action, but rather occurred as a consequence of ovarian steroid production during stimulation. In particular, during COH, estrogen is known to increase progressively to achieve substantial circulating concentrations that are inversely related to declining AMH levels (21). In infertile women, Fanchin et al. (21) showed that decreases in serum AMH were accompanied by increases in E2 levels during COH, which was attributed to the probable loss of small antral follicles subjected to high-dose gonadotropin therapy, although an effect of rising E2 levels was also considered a possibility. In contrast, in PCOS and normal infertile women undergoing COH, a reduction in AMH levels was observed by Eldar-Geva et al. (12), although increased E2 levels at the time of human chorionic gonadotropin were similar among groups. As previously mentioned, Baarends et al. (2) showed that estradiol benzoate inhibited AMH and AMH type II receptor mRNA expression in preantral and small antral follicles of treated immature rats. Consistent with these results is the recent report of an inverse relationship between follicular fluid concentrations of AMH and E2 in small antral follicles retrieved from normogonadotropic women with a cancer diagnosis (24). Based on these observations, an effect of rising estrogen during continuous FSH stimulation may have contributed, in part, to the corresponding decrease in serum AMH detected during COH. By comparison, the short-term nature of our study may have precluded an effect of FSH and estrogen on serum AMH production.

In summary, we have determined that AMH levels remained relatively unchanged over a 24-h period after acute FSH stimulation in women with PCOS and normal women. Within PCOS women, the basal and stimulated AMH levels were significantly greater than those in normal women. The results of this study demonstrate that acute exposure to FSH does not appear to influence AMH expression. Further investigation into the regulation of AMH is necessary for a more comprehensive understanding of its role in ovarian physiology and function.


   Acknowledgments
 
We are grateful to Mr. Jeff Wong for his technical expertise and to the nurses and staff of the University of California, San Diego, General Clinical Research Center for their dedicated care.


   Footnotes
 
This research was supported by the National Institute of Child Health and Human Development/National Institutes of Health (NIH) through a cooperative agreement (U54 HD 12303-20) as part of the Specialized Cooperative Centers Program in Reproduction Research and in part by NIH Grant MO1 RR00827.

Disclosure Statement: D.S.W., M.S.C., P.J.M., and R.J.C. have nothing to declare.

First Published Online February 13, 2007

Abbreviations: A, Androstenedione; AMH, anti-Mullerian hormone; COH, controlled ovarian hyperstimulation; CV, coefficient(s) of variation; DHEAS, dehydroepiandrosterone sulfate; E1, estrone; E2, estradiol; 17-OHP, 17-hydroxyprogesterone; P4, progesterone; PCOS, polycystic ovary syndrome; r-hFSH, recombinant human FSH; T, testosterone.

Received November 6, 2006.

Accepted February 5, 2007.


   References
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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