Link Between Nutrition, AMH, and Adipokines Levels in PCOS
Link Between Nutrition, AMH, and Adipokines Levels in PCOS
Objective The aim of the study was to analyse the relationship between nutritional status, selected adipokines and plasma anti-Müllerian hormone (AMH) levels in women with polycystic ovary syndrome (PCOS).
Study Design Patients and Measurements A prospective, cross-sectional study, involving 87 PCOS (48 obese) women and 67 non-PCOS women (36 obese). Anthropometric parameters were measured, and body composition was determined by the bioimpedance method. Fasting serum glucose, androgens, FSH, LH, SHBG, insulin, AMH, apelin-36, adiponectin, leptin and omentin-1 were measured.
Results Plasma AMH levels were significantly higher in PCOS compared to the non-PCOS group (7·8 ± 4·3 ng/ml vs 4·4 ± 2·4 ng/ml; P < 0·001). Furthermore, AMH levels were higher in both PCOS and non-PCOS normal weight than in obese subgroups (8·9 ± 4·4 ng/ml vs 7·0 ± 4·0 ng/ml; P < 0·05 and 5·1 ± 2·4 ng/ml vs 3·9 ± 2·3 ng/ml; P < 0·05). There were negative correlations between AMH levels and anthropometric parameters (body mass, BMI, fat mass and percentage, as well as waist circumference) and plasma omentin-1 concentrations (R = −0·28, P < 0·001; R = −0·30, P < 0·001; R = −0·36, P < 0·001; R = −0·34, P < 0·001; R = −0·23, P < 0·01; and R = −0·20, P < 0·05, respectively) in all study groups. In multiple regression analysis, circulating AMH level variability was explained by omentin-1 levels and anthropometric parameters (excluding waist circumference).
Conclusions In this observational study, nutritional status appears to be the main factor influencing circulating AMH levels independent of PCOS. The observed AMH association with omentin-1 levels suggests that this adipokine may be a link between hormonal dysfunction of adipose tissue related to obesity and decreased AMH secretion.
Anti-Müllerian hormone (AMH) produced by granulosa cells of primary, preantral and small antral follicles is recognized as a marker of ovarian reserve. This hormone suppresses growing follicles by inhibition of follicle-stimulating hormone (FSH)-dependent aromatase expression and activation of luteinizing hormone (LH) receptors.
AMH ovary secretion and plasma levels are age dependent. The highest AMH values are observed in pubertal age. They decrease slowly from the age of 25 years, are substantially lower in the premenopausal period, and not detectable after the menopause. Furthermore, it was found that plasma AMH level is related to ovarian follicle count. It was also observed that in polycystic ovaries the AMH production in granulosa cells is 75 times greater than in normal ovaries, and plasma AMH levels in PCOS women are 2–3 times higher than in healthy women. Thus, it was suggested that AMH level is a marker of the severity of ovulatory disturbances in PCOS.
Some previously published results indicate that nutritional status may influence circulating AMH levels. Lower plasma AMH levels were found in obese compared to normal weight non-PCOS women, and an inverse association between AMH levels and BMI values was shown. This may reflect a decreased ovarian reserve and fertility in obese women along with a decreased response to gonadotropin stimulation during superovulation. It has also been suggested that obesity directly influences ovarian AMH synthesis. Additionally, Su et al. proposed that lower AMH levels in late reproductive age obese women are the effect of other physiologic processes independent on antral follicle count. In contrast, other studies revealed that nutritional status (defined according to WHO BMI criteria: underweight, normal weight, overweight and obesity) did not affect serum AMH levels in reproductive age and premenopausal women.
The contradictory results have also been obtained in studies that assessed the relationship between nutritional status and AMH level in PCOS women. Some authors have described lower AMH levels in obese PCOS women and an inverse association between AMH levels and BMI, while other did not show relation between AMH and nutritional status in PCOS or even positive correlation between AMH levels and BMI values.
A recently published study has shown that leptin but not adiponectin may affect the AMH synthesis and signalling by the JAK2/STAT3 pathway in infertile women undergoing fresh IVF and ICSI cycles. There seems to be an inverse association between insulin levels, HOMA-IR values, circulating RBP4 and AMH, as well as a positive correlation between AMH and adiponectin. So far, there is a lack of studies that assess the relationships between circulating AMH and adipokines levels in PCOS. Our previously published studies revealed changes of circulating adiponectin, apelin, leptin and omentin-1 levels in PCOS.
The aim of the study was to analyse the relationship between nutritional status, selected plasma adipokines and AMH levels in PCOS women.
Abstract and Introduction
Abstract
Objective The aim of the study was to analyse the relationship between nutritional status, selected adipokines and plasma anti-Müllerian hormone (AMH) levels in women with polycystic ovary syndrome (PCOS).
Study Design Patients and Measurements A prospective, cross-sectional study, involving 87 PCOS (48 obese) women and 67 non-PCOS women (36 obese). Anthropometric parameters were measured, and body composition was determined by the bioimpedance method. Fasting serum glucose, androgens, FSH, LH, SHBG, insulin, AMH, apelin-36, adiponectin, leptin and omentin-1 were measured.
Results Plasma AMH levels were significantly higher in PCOS compared to the non-PCOS group (7·8 ± 4·3 ng/ml vs 4·4 ± 2·4 ng/ml; P < 0·001). Furthermore, AMH levels were higher in both PCOS and non-PCOS normal weight than in obese subgroups (8·9 ± 4·4 ng/ml vs 7·0 ± 4·0 ng/ml; P < 0·05 and 5·1 ± 2·4 ng/ml vs 3·9 ± 2·3 ng/ml; P < 0·05). There were negative correlations between AMH levels and anthropometric parameters (body mass, BMI, fat mass and percentage, as well as waist circumference) and plasma omentin-1 concentrations (R = −0·28, P < 0·001; R = −0·30, P < 0·001; R = −0·36, P < 0·001; R = −0·34, P < 0·001; R = −0·23, P < 0·01; and R = −0·20, P < 0·05, respectively) in all study groups. In multiple regression analysis, circulating AMH level variability was explained by omentin-1 levels and anthropometric parameters (excluding waist circumference).
Conclusions In this observational study, nutritional status appears to be the main factor influencing circulating AMH levels independent of PCOS. The observed AMH association with omentin-1 levels suggests that this adipokine may be a link between hormonal dysfunction of adipose tissue related to obesity and decreased AMH secretion.
Introduction
Anti-Müllerian hormone (AMH) produced by granulosa cells of primary, preantral and small antral follicles is recognized as a marker of ovarian reserve. This hormone suppresses growing follicles by inhibition of follicle-stimulating hormone (FSH)-dependent aromatase expression and activation of luteinizing hormone (LH) receptors.
AMH ovary secretion and plasma levels are age dependent. The highest AMH values are observed in pubertal age. They decrease slowly from the age of 25 years, are substantially lower in the premenopausal period, and not detectable after the menopause. Furthermore, it was found that plasma AMH level is related to ovarian follicle count. It was also observed that in polycystic ovaries the AMH production in granulosa cells is 75 times greater than in normal ovaries, and plasma AMH levels in PCOS women are 2–3 times higher than in healthy women. Thus, it was suggested that AMH level is a marker of the severity of ovulatory disturbances in PCOS.
Some previously published results indicate that nutritional status may influence circulating AMH levels. Lower plasma AMH levels were found in obese compared to normal weight non-PCOS women, and an inverse association between AMH levels and BMI values was shown. This may reflect a decreased ovarian reserve and fertility in obese women along with a decreased response to gonadotropin stimulation during superovulation. It has also been suggested that obesity directly influences ovarian AMH synthesis. Additionally, Su et al. proposed that lower AMH levels in late reproductive age obese women are the effect of other physiologic processes independent on antral follicle count. In contrast, other studies revealed that nutritional status (defined according to WHO BMI criteria: underweight, normal weight, overweight and obesity) did not affect serum AMH levels in reproductive age and premenopausal women.
The contradictory results have also been obtained in studies that assessed the relationship between nutritional status and AMH level in PCOS women. Some authors have described lower AMH levels in obese PCOS women and an inverse association between AMH levels and BMI, while other did not show relation between AMH and nutritional status in PCOS or even positive correlation between AMH levels and BMI values.
A recently published study has shown that leptin but not adiponectin may affect the AMH synthesis and signalling by the JAK2/STAT3 pathway in infertile women undergoing fresh IVF and ICSI cycles. There seems to be an inverse association between insulin levels, HOMA-IR values, circulating RBP4 and AMH, as well as a positive correlation between AMH and adiponectin. So far, there is a lack of studies that assess the relationships between circulating AMH and adipokines levels in PCOS. Our previously published studies revealed changes of circulating adiponectin, apelin, leptin and omentin-1 levels in PCOS.
The aim of the study was to analyse the relationship between nutritional status, selected plasma adipokines and AMH levels in PCOS women.
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