Clinical features and circulating gonadotropin, insulin, and androgen interactions in women with polycystic ovarian disease

Anttila, Leena; Ding, Ying-Qing; Ruutiainen, Kristiina; Erkkola, Risto; Irjala, Kerttu; Huhtaniemi, Ilpo

doi:10.1016/s0015-0282(16)54352-0

Cited by 69 publications

(18 citation statements)

References 24 publications

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“…Several studies have investigated the relationship between body fat and inappropriate gonadotropin secretion in PCOS (9)(10)(11)43). One proposal is that an obesity-associated factor suppresses GnRH pulse amplitude or pituitary responsiveness, but not pulse frequency in this syndrome (10,11).…”

Section: Figurementioning

confidence: 99%

Augmented frequency and mass of LH discharged per burst are accompanied by marked disorderliness of LH secretion in adolescents with polycystic ovary syndrome

Garcia-Rudaz

Ropelato

Escobar

et al. 1998

European Journal of Endocrinology

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The aim of this study was to quantify pulsatile LH secretion, burst frequency and mass, LH half-life, and the approximate entropy (ApEn) or (dis-) orderliness of LH release in adolescents with polycystic ovary syndrome (PCOS), combining a high-precision immunofluorimetric LH assay with deconvolution techniques.We sampled LH concentration profiles every 20 min overnight in 12 girls with PCOS (mean Ϯ S.E.M. age 16.4 Ϯ 0.57 years, body mass index (BMI) 24.4 Ϯ 1.6 kg/m 2 ) and 11 eumenorrheic earlyfollicular-phase controls (mean Ϯ S.E.M. age 16.5 Ϯ 0.47 years, BMI 22.2 Ϯ 1.0 kg/m 2 ). Fasting serum levels of androstenedione, testosterone, 17-hydroxyprogesterone (17-OHP), estrone. estradiol, FSH and sex hormone-binding globulin (SHBG) were determined. Compared with euandrogenic girls, PCOS adolescents had significantly (P < 0.005) elevated serum LH/FSH ratios, 17-OHP, androstenedione, esterone and testosterone levels, decreased SHBG, and similar estradiol. PCOS subjects exhibited a 3-fold higher mean serum LH concentration with almost no overlap with controls (8.8 Ϯ 1.2 and 2.8 Ϯ 0.3 IU/l respectively, P < 0.001). We initially used a conventional serum hormone concentration peak analysis method (Cluster) to evaluate the characteristics of pulsatile LH release. Cluster analysis disclosed a significant increase in serum LH concentration maximal peak height, a higher LH peak frequency and a higher mean serum LH concentration in interpulse nadirs in the PCOS group. Deconvolution analysis of mechanisms underlying the foregoing showed higher frequency in the PCOS group than the controls (7.9 Ϯ 0.4 and 5.7 Ϯ 0.6 pulses/12 h respectively, P < 0.05). The mass of LH released per secretory event was also significantly higher in PCOS subjects than controls (5.4 Ϯ 0.57 and 3.4 Ϯ 0.56 IU/l respectively, P < 0.05). Since the pulsatile production rate is the product of the mean mass of hormone secreted per pulse and the number of pulses per day, we estimated a significantly higher mean pulsatile production rate of (endogenous) LH in the PCOS group (41 Ϯ 4.2 IU/l per day in the PCOS group vs 18 Ϯ 2.3 IU/l per day in the controls, P < 0.01). The mean estimated half-life of endogenous LH disappearance was also significantly higher in patients with PCOS than in controls (110 Ϯ 8.5 and 77 Ϯ 3.7 min respectively, P < 0.01). To quantify the orderliness of LH release, we used ApEn. PCOS patients had remarkably increased disorderliness (higher ApEn) of LH release (1.09 Ϯ 0.04 vs 0.77 Ϯ 0.08 in controls, P ¼ 0.002). Mean serum LH concentration, mass of LH secreted per burst, and LH production rate in PCOS, but not in normal adolescents, correlated positively with androstenedione (P < 0.02, 0.02 and 0.05 respectively). The same parameters also correlated positively with 17-OHP (P < 0.05, 0.02 and 0.05 respectively). Stepwise regression analysis unmasked a negative influence of BMI in PCOS on both mass of LH secreted per burst (r ¼ ¹0.77, P < 0.005) and LH production rate (r ¼ ¹0.70, P < 0.01). We conclude that PCOS adolescents secrete ...

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Section: Figurementioning

confidence: 99%

Augmented frequency and mass of LH discharged per burst are accompanied by marked disorderliness of LH secretion in adolescents with polycystic ovary syndrome

Garcia-Rudaz

Ropelato

Escobar

et al. 1998

European Journal of Endocrinology

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“…But some failed to find such a relationship 21,17,22 . Hyperandrogenism and polycystic ovaries are commonly found in extreme IR 23,3 .…”

Section: Methodsmentioning

confidence: 99%

“…Fasting plasma glucose was estimated by glucose oxidase method 14 , S. insulin by Abbott AxSym system on MEIA principle 15 , S. free testosterone by ELISA 16 . Insulin resistance (IR) was calculated by using the formula: (fastng glucose: fasting insulin ratio), with a value <4.5 taken as a measure of IR 17 . All statistical analyses were done by SPSS, version 12.0.…”

Section: Introductionmentioning

confidence: 99%

Characteristics of Insulin and Androgen Status in Polycystic Ovary Syndrome

Banu

Wahab

Debnath

et al. 2013

Bangladesh J Med Biochem

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hirsutism, acne or male pattern balding) and c) exclusion of hyperprolactinemia, nonclassical adrenal hyperplasia and thyroid disorders 1 . Burghen et al (1980) reported both basal and glucose stimulated hyperinulinemia in women with PCOS 2 . Many investigators found hyperinsulinemia and hyperandrogenemia are co-existent in PCOS 3 . IntroductionAccording to National Institute of Health (1990) ABSTRACTPolycystic Ovary Syndrome (PCOS) was originally described as a syndrome of amenorrhea, hirsutism and obesity associated with enlarged polycystic ovaries. There is increased androgen level and in some, insulin resistance (IR). Etiological relationship of androgen excess and IR in PCOS is not established. Influence of obesity on PCOS is controversial. This study was designed to see the androgen and insulin status in PCOS among obese and non-obese patients. It was a case-control study. Of total 80 study subjects, 60 primary infertile women suffering from PCOS were cases (30 obese and 30 non-obese). Age and BMI matched 20 healthy women having normal menstrual cycles were controls (10 obese and 10 non-obese). Age range of all were 20-40 years. Fasting plasma glucose, fasting S. Insulin and free Testosterone were measured. Insulin resistance (IR) was assessed by fasting glucose to insulin ratio (<4.5). Subjects with DM or known endocrine disorders that may be associated with abnormal S.Insulin or plasma glucose concentration were excluded. No significant difference of fasting plasma glucose between PCOS (obese or non-obese) and respective controls (P>0.5, in each) were observed. Significant difference of fasting S. Insulin and testosterone were observed between PCOS (both obese and non-obese) and respective controls (P<0.01 in each), but there was no significant difference between obese and non-obese PCOS (P>0.05). There was no significant difference of S.Testosterone between obese and non-obese PCOS(P>0.05). There was also no significant difference of IR between obese and non-obese PCOS, but the ratio was <4.5 (indicating IR in both). There were no significant correlation of S.Insulin with Testosterone in any group of PCOS (obese and non-obese) (P>0.05). Increased S.Insulin and Testosterone was seen in PCOS irrespective of BMI. Further studies with larger sample size is recommended to assess etiological relationship between insulin and testosterone in PCOS.

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“…In-vivo manipulation of insulin concentrations in humans, however, has no effect on measurements of LH pulsatility or LH response to GnRH (Nestler et al, 1989;Dunaif & Graf, 1989). Also, circulating serum insulin and LH concentrations have an inverse relationship Attila et al, 1991). Women with raised LH have normal serum insulin concentrations and hyperinsulinaemic women tend not to hypersecrete LH.…”

Section: Luteinizing Hormonementioning

confidence: 99%