Aim: The aims of the study were to understand the association between insulin-like factor 3 (INSL3) and functional ovarian hyperandrogenism (FOH) in PCOS and the regulatory role played by LH. Subjects and methods: Fifteen PCOS women were classified as FOH (FOH-PCOS, no.=8) and non-FOR (NFOH-PCOS, no.=7) according to the response of 17OH-progesterone to buserelin (a GnRH analogue) with respect to 15 controls. FOH-PCOS and NFOH-PCOS were compared for basal INSL3 levels. In addition, the effect of buserelin on INSL3 concentrations and the relationship between basal and buserelin-stimulated LH and 17OH-progesterone and INSL3 were evaluated. Results: Basal INSL3 levels were higher in FOH-PCOS than NFOH-PCOS (p=0.001) and controls (p=0.001), whereas they did not differ between NFOH-PCOS and controls. In addition, FOH-PCOS had a higher response of LH to buserelin with respect to NFOH-PCOS. Within all PCOS women the levels of INSL3 positively correlated with free testosterone (p=0.022) and negatively with SHBG (r= p=0.031). Moreover, positive correlations with the absolute increase of 17OH-progesterone (p<0.001) and with the LH area under the curve (p=0.001) after buserelin administration were found. In the multiple regression analysis INSL3 persisted significantly correlated only with 17OH-progesterone response to buserelin. Finally, INSL3 was not significantly modified after buserelin administration either in FOH-PCOS or in NFOH-PCOS. Conclusions: These data suggest that INSL3 is related to FOH in PCOS women, but this association seems not to be mediated by LH, further reinforcing the concept that a pathophysiological heterogeneity for ovarian hyperandrogenism in PCOS exists.

Gambineri A, Patton L, Prontera O, Fanelli F, Ciampaglia W, Cognigni GE, et al. (2011). Basal insulin-like factor 3 levels predict functional ovarian hyperandrogenism in the polycystic ovary syndrome. JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION, 34, 685-691 [10.3275/7726].

Basal insulin-like factor 3 levels predict functional ovarian hyperandrogenism in the polycystic ovary syndrome.

GAMBINERI, ALESSANDRA;PRONTERA, OLGA;FANELLI, FLAMINIA;PAGOTTO, UBERTO;PASQUALI, RENATO
2011

Abstract

Aim: The aims of the study were to understand the association between insulin-like factor 3 (INSL3) and functional ovarian hyperandrogenism (FOH) in PCOS and the regulatory role played by LH. Subjects and methods: Fifteen PCOS women were classified as FOH (FOH-PCOS, no.=8) and non-FOR (NFOH-PCOS, no.=7) according to the response of 17OH-progesterone to buserelin (a GnRH analogue) with respect to 15 controls. FOH-PCOS and NFOH-PCOS were compared for basal INSL3 levels. In addition, the effect of buserelin on INSL3 concentrations and the relationship between basal and buserelin-stimulated LH and 17OH-progesterone and INSL3 were evaluated. Results: Basal INSL3 levels were higher in FOH-PCOS than NFOH-PCOS (p=0.001) and controls (p=0.001), whereas they did not differ between NFOH-PCOS and controls. In addition, FOH-PCOS had a higher response of LH to buserelin with respect to NFOH-PCOS. Within all PCOS women the levels of INSL3 positively correlated with free testosterone (p=0.022) and negatively with SHBG (r= p=0.031). Moreover, positive correlations with the absolute increase of 17OH-progesterone (p<0.001) and with the LH area under the curve (p=0.001) after buserelin administration were found. In the multiple regression analysis INSL3 persisted significantly correlated only with 17OH-progesterone response to buserelin. Finally, INSL3 was not significantly modified after buserelin administration either in FOH-PCOS or in NFOH-PCOS. Conclusions: These data suggest that INSL3 is related to FOH in PCOS women, but this association seems not to be mediated by LH, further reinforcing the concept that a pathophysiological heterogeneity for ovarian hyperandrogenism in PCOS exists.
2011
Gambineri A, Patton L, Prontera O, Fanelli F, Ciampaglia W, Cognigni GE, et al. (2011). Basal insulin-like factor 3 levels predict functional ovarian hyperandrogenism in the polycystic ovary syndrome. JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION, 34, 685-691 [10.3275/7726].
Gambineri A; Patton L; Prontera O; Fanelli F; Ciampaglia W; Cognigni GE; Pagotto U; Pasquali R.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/119561
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