The natural history of the metabolic syndrome in young women with the polycystic ovary syndrome and the effect of long‐term oestrogen–progestagen treatment

Pasquali, Renato; Gambineri, Alessandra; Anconetani, B.; Vicennati, Valentina; Colitta, Donatella; Caramelli, Elisabetta; Casimirri, Francesco; Morselli-Labate, Antonio Maria

doi:10.1046/j.1365-2265.1999.00701.x

Cited by 142 publications

(84 citation statements)

References 45 publications

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“…However, regardless of alterations of insulin secretion, in a 10 y follow-up study we found that both fasting and glucose-stimulated insulin and C-peptide tended to further significantly increase in PCOS women, suggesting a worsened insulin resistant state with time. 77 In the same study we also found that several women developed impaired glucose tolerance. Longitudinal data are therefore warranted to investigate which factor, namely progressive insulin resistance and=or subtle alterations of insulin secretion, may predict the well-documented susceptibility of obese PCOS women toward type 2 diabetes.…”

Section: Androgen Abnormalitiessupporting

confidence: 59%

“…114 In addition, by investigating the long-term effect of oral contraceptive therapy on metabolism and body composition in a group of PCOS women we found a significant reduction of waist circumference and of WHR, as well as of basal insulin levels and an improvement of glucose tolerance in some subjects. 77 These favorable effects were not, however, observed in a group of non-treated women, who had worsened fasting and glucose-stimulated insulin levels. Although controversy still exists concerning the effect of oral contraceptive preparations on glucose metabolism and insulin secretion and action in non-PCOS women, the results of this study indicate a potential benefit of long-term estroprogestagen compounds in body composition and the glucose-insulin system at least in PCOS women.…”

Section: Other Drugsmentioning

confidence: 90%

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Obesity and the polycystic ovary syndrome

et al. 2002

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The polycystic ovary syndrome (PCOS) is a condition characterized by hyperandrogenism and chronic oligo-anovulation. However, many features of the metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are overweight or obese and most of them have the abdominal phenotype. Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and an increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Other factors such as increased estrogen production rate, increased activity of the opioid system and of the hypothalamic-pituitary-adrenal axis, decreased sex hormone binding globulin synthesis and, possibly, high dietary lipid intake, may be additional mechanisms by which obesity favours the development of hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features (such as hirsutism, menstrual abnormalities and anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype.Body weight loss is associated with beneficial effects on hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding insulin-sensitizing agents and=or antiandrogens to weight reduction programmes. These obviously emphasize the role of obesity in the pathophysiology of PCOS.

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Section: Androgen Abnormalitiessupporting

confidence: 59%

Section: Other Drugsmentioning

confidence: 90%

Obesity and the polycystic ovary syndrome

et al. 2002

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“…IR constitutes a prerequisite for diabetes mellitus (DM) and/or metabolic syndrome development, and consequently the increased incidence of these two morbidities in women with PCOS, compared with their BMI-matched peers, is expected (5,6,7,8,9). However, the available prospective studies reporting the significantly higher incidence of DM in women with PCOS compared with general population are few and DM is found mainly in obese women with the syndrome (10,11,12).…”

Section: Introductionmentioning

confidence: 87%

Diverse impacts of aging on insulin resistance in lean and obese women with polycystic ovary syndrome: evidence from 1345 women with the syndrome

Livadas

Panidis

Diamanti-Kandarakis

2014

European Journal of Endocrinology

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Background: Polycystic ovary syndrome (PCOS) represents a moving spectrum of hormonal to metabolic abnormalities, as women with the syndrome are aging. Hormonal abnormalities, anovulation, and hyperandrogenic signs were predominant during the early years of PCOS and fade away with the years. Metabolic abnormalities and insulin resistance (IR) remain throughout the PCOS life cycle; however, it is unclear as to how they change, as women with the syndrome are aging. Objective: To evaluate the changes in IR and its associations with clinical, biochemical, hormonal, and ultrasound findings in a large cohort of women with PCOS and controls, as they are aging. Design: A cross-sectional study was carried out to evaluate the diverse impacts of aging on IR. Setting: An outpatient clinic was chosen for the study. Participants: A total of 1345 women with PCOS (Rotterdam criteria) and 302 controls of Caucasian origin and Greek ethnicity comprised the study group. Main outcome and measures: The impact of age on IR, as calculated using homeostasis model assessment of IR (HOMA-IR) index, and several PCOS characteristics were evaluated. Results: In PCOS, age (K0.045G0.008) was negatively, and BMI positively (0.18G0.007) associated with HOMA-IR (R 2 Z0.36).

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“…Plasma glucose levels were determined by the glucose oxidase technique immediately after blood was drawn. Levels for insulin, total testosterone, DHEA and its sulfate (DHEA-S), androstenedione, 17-OHP, SHBG, and cortisol were determined as previously described (18,27,28). The intra-assay coefficients of variation in our laboratory were 3.0% for insulin, 7.0% for total testosterone, 9.0% for DHEA, 5.9% for DHEA-S, 6.0% for androstenedione, 13.0% for 17-OHP, 6.5% for SHBG, and Ͻ8.0% for cortisol.…”

mentioning

confidence: 99%

Glucose Intolerance in a Large Cohort of Mediterranean Women With Polycystic Ovary Syndrome

et al. 2004

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The aim of this study was to investigate the phenotypic parameters and associated factors characterizing the development of glucose intolerance in polycystic ovary syndrome (PCOS). Among the 121 PCOS female subjects from the Mediterranean region, 15.7 and 2.5% displayed impaired glucose tolerance and type 2 diabetes, respectively. These subjects were included in a single group of overweight or obese subjects presenting with glucose intolerance (GI) states. PCOS women with normal glucose tolerance (81.8%) were subdivided into two groups: those who were overweight or obese and those of normal weight. Metabolic and hormonal characteristics of the GI group included significantly higher fasting and glucose-stimulated insulin levels, more severe insulin resistance, hyperandrogenemia, and significantly higher cortisol and androstenedione responses to 1-24 ACTH stimulation. One important finding was that lower birth weight and earlier age of menarche were associated with GI in PCOS women. Frequency of hirsutism, oligomenorrhea, acne, and acanthosis nigricans did not characterize women with GI. Our findings indicate that PCOS patients with GI represent a subgroup with specific clinical and hormonal characteristics. Our observations may have an important impact in preventative and therapeutic strategies. Diabetes 53: 2353-2358, 2004 P olycystic ovary syndrome (PCOS) affects 5-10% of women during their reproductive age (1,2) and is one of the most common causes of female infertility (1). The major clinical manifestations of the syndrome in adults are chronic anovulation, menstrual abnormalities, and hyperandrogenism (1). Most PCOS women present with insulin resistance and hyperinsulinemia (1), which play an important role in the pathogenesis of PCOS by modulating both ovarian and adrenal androgen production and decreasing sex hormoneϪbinding globulin (SHBG) liver synthesis and blood levels (3).Studies in American and Asian subjects have shown that, compared with the general population, women with PCOS have an increased risk for impaired glucose tolerance (IGT) and type 2 diabetes (4 -6), with a tendency toward early development of glucose intolerance (GI) states (7). However, to our knowledge, no studies have been performed on subjects from the Mediterranean region. The strong connection between PCOS and GI states is further emphasized by the high prevalence of polycystic ovarian morphology found on ultrasound scans in premenopausal women with type 2 diabetes (8) and those with previous gestational diabetes (9).As has been seen in the general population (10), there is evidence that insulin resistance may play a major pathophysiological role in the development of GI in PCOS women (11,12). The decreased insulin sensitivity in PCOS women appears in fact quite similar to that found in type 2 diabetic patients and to be relatively independent of obesity, fat distribution, and lean body mass (13). On the other hand, there is strong evidence that obesity per se, particularly the abdominal phenotype, represents an important indepe...

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The natural history of the metabolic syndrome in young women with the polycystic ovary syndrome and the effect of long‐term oestrogen–progestagen treatment

Cited by 142 publications

References 45 publications

Obesity and the polycystic ovary syndrome

Obesity and the polycystic ovary syndrome

Diverse impacts of aging on insulin resistance in lean and obese women with polycystic ovary syndrome: evidence from 1345 women with the syndrome

Glucose Intolerance in a Large Cohort of Mediterranean Women With Polycystic Ovary Syndrome

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