Prorenin is elevated in polycystic ovary syndrome and may reflect hyperandrogenism

Morris, Randy S.; Wong, I. Lane; Hatch, I.; Gentschein, Elizabeth; Paulson, Richard J.; Løbo, Rogerio A.

doi:10.1016/s0015-0282(16)57967-9

Cited by 24 publications

(16 citation statements)

References 19 publications

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“…The ovarian RAS can induce hyperandrogenism and contribute to the manifestation of PCOS. It is also known that baseline levels of renin are elevated in women with PCOS and correlate with serum androgen levels (32,33). Prorenin production has been detected in the theca cells (34), while the cystic follicles in PCOS have demonstrated increased production of renin and angiotensin II from theca and granulosa cells, as occurs in normal atretic ovarian follicles (35).…”

Section: Discussionmentioning

confidence: 99%

Increased frequency of the DI genotype of the angiotensin-I converting enzyme and association of the II genotype with insulin resistance in polycystic ovary syndrome

Koika

Georgopoulos

Piouka

et al. 2012

European Journal of Endocrinology

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Objective: The polycystic ovary syndrome (PCOS) is a common and complex disease with unclear pattern of inheritance, characterized by an androgen excess, while hyperinsulinemia and insulin resistance (IR) are common features of the syndrome. The angiotensin I converting enzyme (ACE) insertion (I)/deletion (D) gene polymorphism was proved to be involved in many pathophysiological conditions, including hypertension and IR. Design: The purpose of this study was to evaluate the involvement of the ACE gene polymorphism in the pathogenesis of PCOS. Methods: In a case-control association study involving 801 PCOS women and 266 healthy controls, hormonal determinations and ACE polymorphism genotyping were performed. The PCOS women were classified into three groups: Group A presented biochemical hyperandrogenism, combined with anovulation and polycystic ovarian morphology; Group B, clinical hyperandrogenism combined with anovulation and polycystic ovarian morphology; and Group C, chronic anovulation and polycystic ovarian morphology. Results: A significant increase in the frequency of the DI genotype of the ACE polymorphism was detected in PCOS women as a whole (PZ0.035), in PCOS Group A (PZ0.039) and Group B (PZ0.010), while there was no difference in Group C (PZ0.939). Significant difference was also observed in hyperandrogenic PCOS women as a whole (Group ACB) (PZ0.017). The II genotype was positively correlated with HOMA-IR and QUICKI and with fasting insulin and glucose/insulin ratio in these groups. Conclusions: The association study of the ACE I/D polymorphism in PCOS women demonstrates an increase in the DI genotype incidence and an association of the II genotype with IR.

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Section: Discussionmentioning

confidence: 99%

Increased frequency of the DI genotype of the angiotensin-I converting enzyme and association of the II genotype with insulin resistance in polycystic ovary syndrome

Koika

Georgopoulos

Piouka

et al. 2012

European Journal of Endocrinology

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“…This finding could be shown to be of clinical significance since the decrease of hyperreninemia could further improve insulin resistance and hyperandrogenemia. In addition, this beneficial effect of metformin might contribute to ovulation improvement in PCOS patients, since it has been shown that ovulation occurred more frequently in PCOS patients receiving clomiphene citrate when baseline levels of renin were reduced [58] . Although ovulation was not assessed, as it was beyond the scope of this study, it may be suggested that the reduction of hyperreninemia induced by metformin may contribute to improvement of ovulation observed after metformin treatment in PCOS women.…”

Section: Discussionmentioning

confidence: 99%

Hyperreninemia Characterizing Women with Polycystic Ovary Syndrome Improves after Metformin Therapy

Diamanti-Kandarakis

Economou²,

Livadas³

et al. 2009

Kidney Blood Press Res

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Background: Polycystic ovary syndrome (PCOS) is characterized by chronic anovulation, hyperandrogenemia and insulin resistance. Hyperreninemia is observed in insulin resistance and hyperandrogenemic states. Aims: To investigate the levels of total plasma renin and their possible relationship with insulin resistance and hyperandrogenemia and to explore the effect of metformin on these parameters in PCOS women. Methods: 48 PCOS women who were age- and body mass index (BMI)-matched with 21 healthy women were studied. Total renin, aldosterone levels, glucose and insulin levels were measured at basal state and during an oral glucose tolerance test in all subjects. A subgroup of women with PCOS was evaluated 6 months after metformin administration. Results: Total renin levels were significantly higher in PCOS women compared to controls. PCOS women compared to controls displayed higher areas under the curve for glucose, insulin and total renin (AUCREN). Mean AUCREN was correlated significantly with insulin resistance indices and positively with free testosterone levels. Total renin, aldosterone, androgen levels and insulin sensitivity indices were significantly improved after 6 months on metformin treatment. Conclusions: PCOS women demonstrated an insulin resistance and hyperandogenemia-related increase in serum total renin levels. Metformin treatment was shown to significantly reduce total renin levels.

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“…In women with PCOS, plasma renin activity was found to be elevated compared with a control group [Uncu et al 2002]. Plasma prorenin has also been shown to be higher in women with PCOS and correlates positively with serum androgen levels [Morris et al 1995]. However, there is also evidence for involvement of the endothelin (ET)-system in PCOSassociated hypertension: ET-1 has been found in human follicular fluid, and ET-1 mRNA expression has been found in ovarian tissues [Gentili et al 2001].…”

Section: Polycystic Ovary Syndromementioning

confidence: 99%

Review: The metabolic syndrome as an endocrine disease: is there an effective pharmacotherapeutic strategy optimally targeting the pathogenesis?

Schindler

2007

Therapeutic Advances in Cardiovascular Disease

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The metabolic syndrome (MetS) represents a combination of cardiovascular risk determinants such as obesity, insulin resistance and lipid abnormalities such as hypertriglyceridemia, increased free fatty acids, low high-density-cholesterol and hypertension. As a multiple component condition it imparts a doubling of relative risk for atherosclerotic cardiovascular disease (ASCVD). It is currently controversial which component of the syndrome carries what weight. There is even a considerable debate whether the risk for ASCVD is greater in patients diagnosed with MetS than that by the individual risk factors. At present, no unifying pathogenetic mechanism can explain the metabolic syndrome and there is no unique treatment for it. This review summarizes and critically reviews the currently available clinical and scientific evidence for the concept that the MetS is causally an endocrine disease and discusses pharmacotherapeutic strategies targeting the pathogenesis rather than single symptoms of the cluster.

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Prorenin is elevated in polycystic ovary syndrome and may reflect hyperandrogenism

Cited by 24 publications

References 19 publications

Increased frequency of the DI genotype of the angiotensin-I converting enzyme and association of the II genotype with insulin resistance in polycystic ovary syndrome

Increased frequency of the DI genotype of the angiotensin-I converting enzyme and association of the II genotype with insulin resistance in polycystic ovary syndrome

Hyperreninemia Characterizing Women with Polycystic Ovary Syndrome Improves after Metformin Therapy

Review: The metabolic syndrome as an endocrine disease: is there an effective pharmacotherapeutic strategy optimally targeting the pathogenesis?

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