Effect of rosiglitazone on insulin resistance, growth factors, and reproductive disturbances in women with polycystic ovary syndrome

Belli, Susana; Graffigna, Mabel; Oneto, Adriana; Otero, Patricia; Schurman, León; Levalle, Oscar

doi:10.1016/j.fertnstert.2003.08.024

Cited by 109 publications

(82 citation statements)

References 55 publications

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“…These differences most likely reflect long-term differences in adrenomedullary function, androgen concentrations, and exposure to glucocorticoids. Our findings are concordant with the results of PCOS patients [33, 34]. No correlation was demonstrated between hyperinsulinemia and leptin.…”

Section: Discussionsupporting

confidence: 92%

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Hyperinsulinemia and Insulin Insensitivity in Women with Nonclassical Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency: The Relationship between Serum Leptin Levels and Chronic Hyperinsulinemia

2005

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Background/Aim: Nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency (NC-CAH) is associated with hyperandrogenemia, chronic anovulation, hirsutism, acne and adrenal hyperplasia. A few studies have shown hyperinsulinemia and insulin insensitivity in NC-CAH. Hyperinsulinemia can stimulate leptin secretion, and androgens can inhibit leptin secretion. Thus, we designed a study to investigate the insulin levels and insulin sensitivity and the effect of chronic endogenous hyperinsulinemia and androgens on leptin in patients with NC-CAH. Methods: Eighteen women with untreated NC-CAH and 26 normally cycling control women with a similar body mass index (BMI) were studied. Basal hormones, fasted and fed insulin levels, leptin and stimulated 17-hydroxyprogesterone (17-OHP) concentrations were studied. Homeostasis model assessment was used to assess insulin sensitivity. Results: The basal 17-OHP, the free testosterone (fT) and dehydroepiandrosterone sulfate (DHEA-S) were significantly different in the 2 groups (p < 0.05). Fasting and fed insulin levels of the NC-CAH group were higher than those of the control group (p < 0.05) and insulin sensitivity was lower in NC-CAH than in controls (p < 0.05). Insulin levels were correlated with fT and 17-OHP (p < 0.05). Serum leptin levels for NC-CAH (25.9 ± 12.5 µg/l) did not differ from the controls (25.4 ± 12.06 µg/l) and were positively correlated with BMI (r = 0.725) and percent body fat (r = 0.710) for both groups (both p < 0.001). Leptin levels were not correlated with estrogen or androgens, gonadotropins or insulin levels. Conclusion: Hyperinsulinemia and insulin insensitivity associated with hyperandrogenism were detected in untreated NC-CAH patients as in previous reports, whereas serum leptin levels did not differ from those of controls.

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Section: Discussionsupporting

confidence: 92%

“…Leptin did not change in cases of hyperandrogenemia or hyperinsulinemia in patients with NC-CAH as in the previous reports on PCOS [34, 35]. …”

Section: Discussionsupporting

confidence: 81%

Hyperinsulinemia and Insulin Insensitivity in Women with Nonclassical Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency: The Relationship between Serum Leptin Levels and Chronic Hyperinsulinemia

2005

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“…Similar data regarding improvement in insulin resistance and hyperinsulinemia, hyperandrogenism and ovulation observed with troglitazone administration were subsequently reported in smaller studies in which obese PCOS women underwent treatment with rosiglitazone (93)(94)(95)(96)(97) and pioglitazone (98,99). Rosiglitazone was found to increase ovulatory frequency and improve hyperandrogenemia even in non-obese women with PCOS with normal insulin sensitivity (100).…”

Section: Thiazolidinedionesmentioning

confidence: 54%

Insulin-sensitizing agents in polycystic ovary syndrome

Pasquali

Gambineri

2006

eur j endocrinol

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Insulin-sensitizing agents have been recently proposed as the therapy of choice for polycystic ovary syndrome (PCOS), since insulin resistance and associated hyperinsulinemia are recognized as important pathogenetic factors of the syndrome. Moreover, since almost all obese PCOS women and more than half of those of normal weight are insulin resistant, and therefore present some degree of hyperinsulinemia, the use of insulin sensitizers should be suggested in most patients with PCOS. Insulin sensitizer treatment has been associated with a reduction in serum androgen levels and gonadotropins, and with an improvement in serum lipids and in prothrombotic factor plasminogenactivator inhibitor type 1, whatever the insulin sensitizer used. This therapy has also been associated with a decrease in hirsutism and acne, and with a regulation of menses and an improvement of ovulation and fertility. Notable improvements in all these parameters have also been described after a change in lifestyle approach, particularly in the presence of obesity. Lifestyle interventions should therefore be combined with insulin sensitizers in PCOS when obesity is present.

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“…It has been proposed that obesity and insulin resistance may amplify rather than cause the reproductive features of PCOS (Walters et al 2012). In clinical trials treatment with insulin sensitizing medications, such as thiazolidinediones and metformin, did not seem to consistently lower leptin concentrations unless there was weight loss (Mantzoros et al 1997b, Belli et al 2004, Romualdi et al 2008, Tfayli et al 2011, further indicating the complexity of the insulin and leptin interplay.…”

Section: Polycystic Ovarian Syndromementioning

confidence: 99%

20 YEARS OF LEPTIN: Role of leptin in human reproductive disorders

Chou¹,

Mantzoros²

2014

Journal of Endocrinology

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Leptin, as a key hormone in energy homeostasis, regulates neuroendocrine function, including reproduction. It has a permissive role in the initiation of puberty and maintenance of the hypothalamic-pituitary-gonadal axis. This is notable in patients with either congenital or acquired leptin deficiency from a state of chronic energy insufficiency. Hypothalamic amenorrhea is the best-studied, with clinical trials confirming a causative role of leptin in hypogonadotropic hypogonadism. Implications of leptin deficiency have also emerged in the pathophysiology of hypogonadism in type 1 diabetes. At the other end of the spectrum, hyperleptinemia may play a role in hypogonadism associated with obesity, polycystic ovarian syndrome, and type 2 diabetes. In these conditions of energy excess, mechanisms of reproductive dysfunction include central leptin resistance as well as direct effects at the gonadal level. Thus, reproductive dysfunction due to energy imbalance at both ends can be linked to leptin.

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Effect of rosiglitazone on insulin resistance, growth factors, and reproductive disturbances in women with polycystic ovary syndrome

Cited by 109 publications

References 55 publications

Hyperinsulinemia and Insulin Insensitivity in Women with Nonclassical Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency: The Relationship between Serum Leptin Levels and Chronic Hyperinsulinemia

Hyperinsulinemia and Insulin Insensitivity in Women with Nonclassical Congenital Adrenal Hyperplasia due to 21-Hydroxylase Deficiency: The Relationship between Serum Leptin Levels and Chronic Hyperinsulinemia

Insulin-sensitizing agents in polycystic ovary syndrome

20 YEARS OF LEPTIN: Role of leptin in human reproductive disorders

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