Hyperinsulinemia and human chorionic gonadotropin synergistically promote the growth of ovarian follicular cysts in rats

Poretsky, Leonid; Clemons, Jeffrey; Bogovich, Katryna

doi:10.1016/0026-0495(92)90175-a

Cited by 85 publications

(58 citation statements)

References 34 publications

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“…The treatment protocol was composed of S.C. injections of saline (control animals), daily 3 IU hCG and insulin in order to obtain a hyperinsulinemic state. Briefly, saline and the hormones were administered twice a day, insulin injections started with 0$5 IU/day and gradually increased to 6 IU/day from the 11th day until the 22nd day (Poretsky et al 1992). On the 23rd day, 14 h after the last hormone administration, the rats were anesthetized with sodium thiopental (25 mg/kg, i.p.…”

Section: Animal Tissue Extractsmentioning

confidence: 99%

Up-regulation of the phosphatidylinositol 3-kinase/protein kinase B pathway in the ovary of rats by chronic treatment with hCG and insulin

Lima

Souza

Caperuto

et al. 2006

Journal of Endocrinology

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Polycystic ovary syndrome (PCOS) manifests as chronic anovulation, ovarian hyperandrogenism, and follicular cysts, which are amplified by insulin as well as the inability of the hormone to stimulate glucose uptake in classic target tissues such as muscle and fat. In the present study, we evaluated the regulation of the insulin-signaling pathways by using immunoprecipitation and immunoblotting in whole extracts of ovaries from non-pregnant human chorionic gonadotropin (hCG)-treated rats, hyperinsulinemic-induced rats and hyperinsulinemic-induced rats, treated with hCG for 22 consecutive days. There were increased associations of insulin receptor substrate (IRS)-1 and IRS-2 with phosphatidylinositol (PI) 3-kinase, followed by enhanced protein kinase B (Akt) serine and threonine phosphorylation, in the ovaries of rats that were treated with hCG, either alone or with insulin. In contrast, the skeletal muscle demonstrated a reduced IRS-1/PI 3-kinase/Akt pathway in hyperinsulinemic-induced rats. These intracellular modifications were accompanied by follicular cysts, detected by optical microscopy, and increased androstenedione serum levels. In summary, our data show that chronic treatment with hCG or hCG plus insulin can induce changes in ovaries that simulate PCOS. In these situations, an increase in the insulin-induced IRS/PI 3-kinase/Akt pathway occurs in the ovary, suggesting that the activation of this pathway may have a role in the development of PCOS.

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Section: Animal Tissue Extractsmentioning

confidence: 99%

Up-regulation of the phosphatidylinositol 3-kinase/protein kinase B pathway in the ovary of rats by chronic treatment with hCG and insulin

Lima

Souza

Caperuto

et al. 2006

Journal of Endocrinology

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“…It should be noted that T1D girls exhibit greater insulin resistance than boys during puberty [25], which may lead to ovarian hyperandrogenism [6]. Poretsky et al [26] showed that the coexistence of hyperinsulinemia and insulin resistance, as observed in T1D girls, leads more frequently to polycystic ovaries than when either phenomenon is present alone.…”

Section: Ovarian Function In T1d (Fig 1)mentioning

confidence: 99%

Puberty and Ovarian Function in Girls with Type 1 Diabetes Mellitus

Codner

Cassorla

2008

Horm Res Paediatr

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Insulin is well known for its effects on carbohydrate metabolism, but this hormone also plays an important role in regulating ovarian function. Granulosa, theca and stromal ovarian cells may be affected by insulin deficiency or excess, which may be present in women with type 1 diabetes mellitus (T1D). Recent publications have shown that in spite of intensive insulin therapy, some delay in the age of thelarche, pubarche and menarche is still observed in girls with T1D. In addition, ovarian hyperandrogenism may be observed during late adolescence and an increased prevalence of hirsutism and polycystic ovarian syndrome (PCOS) has been described in adult women with T1D. These endocrine abnormalities may be related to nonphysiologic insulin replacement therapy and to hyperglycemia. This paper reviews the pubertal development and the clinical reproductive abnormalities observed in girls with type 1 diabetes mellitus, and shows that several significant clinical problems, such as pubertal delay, menstrual disturbances and hyperandrogenism which may ultimately lead to the development of PCOS in adulthood, may be observed in some of these patients.

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“…Pituitary Increases sensitivity to GnRH [36,37] Ovaries Increases the activity of 17,20 lyase [38] Increases the activity of 3β-hydroxysteroid dehydrogenase and aromatase in the granulosa cells [39] Increases LH receptor levels [36,37] Promotes ovarian growth and cyst formation [36,40] Liver Inhibits SHBG production [41] GnRH: Gonadotrophin-releasing hormone; LH: Luteinizing hormone; SHBG: Sex hormone-binding globulin.…”

Section: Target Organ Effect Of Insulinmentioning

confidence: 99%

Obesity Management in Women with Polycystic Ovary Syndrome

Lim

Clifton

Noakes

et al. 2007

Womens Health (Lond Engl)

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Obesity and insulin resistance play an important role in initiating or maintaining ill health in polycystic ovary syndrome (PCOS). This implies that treatment that reduces body weight and insulin resistance would alleviate the symptoms of PCOS. Lifestyle modification has been found to be effective in restoring reproductive function in up to 80% of individuals who achieve at least 5% weight loss. However, long-term weight maintenance is a challenge. This article provides a review of reduced glycemic load diets, including low glycemic index, very low carbohydrate, high-protein and high monounsaturated fat diets, on metabolic and reproductive health in PCOS and non-PCOS populations. Dietary trials in non-PCOS women suggest that higher-protein, reduced glycemic load diets were probably more beneficial than the conventional low-fat, high-carbohydrate diet but further studies are required to confirm this in PCOS women. Similarly, the optimal exercise regime for PCOS women remains to be investigated.Obesity & polycystic ovary syndrome Polycystic ovary syndrome (PCOS) is one of the most common endocrine conditions that affects obese and nonobese women during reproductive age. Its symptoms include irregular menses, infertility, acne and hirsutism (excessive hair growth). During pregnancy, PCOS probably also increases the risk of early miscarriages and complications such as pre-eclampsia and gestational diabetes [1]. As a result of these physical manifestations, women with PCOS tend to have poorer psychological health and lower quality of life [2]. Increasing evidence also suggests that women with PCOS may be at greater risk of developing metabolic diseases such as type 2 diabetes and cardiovascular disease in the long term [3,4].Owing to its heterogeneity, the diagnostic criteria for PCOS have been a contentious issue among experts. The 1990 National Institutes of Health (NIH) meeting defined PCOS as the coexistence of chronic anovulation and hyperandrogenism, with the exclusion of other diseases such as thyroid disorder, hyperprolactinemia, congenital adrenal hyperplasia, androgensecreting tumors and Cushing syndrome [5]. In 2003, this definition was broadened to include women with either hyperandrogenism or anovulation in addition to having polycystic ovaries. Using the previous NIH definition, the prevalence of PCOS was estimated to be 5-8% of women of reproductive age [6][7][8][9]. This number is estimated to increase by 65% using the latest revised diagnostic criteria [10]. Obesity & fat distribution in PCOS womenIt is estimated that 30-60% of women with PCOS are overweight or obese in the Western world [7,[11][12][13][14]. Some suggest that the prevalence of obesity is higher in PCOS women compared with healthy controls [7,15,16]. In a study involving 3094 women, Glueck and colleagues found that approximately 73-78% of women with PCOS aged between 20 and 41 years were obese (body mass index [BMI]>30 kg/m 2 ) compared with 7-14% in the general population [16]. In addition to being potentially predisposed to obesity,...

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Hyperinsulinemia and human chorionic gonadotropin synergistically promote the growth of ovarian follicular cysts in rats

Cited by 85 publications

References 34 publications

Up-regulation of the phosphatidylinositol 3-kinase/protein kinase B pathway in the ovary of rats by chronic treatment with hCG and insulin

Up-regulation of the phosphatidylinositol 3-kinase/protein kinase B pathway in the ovary of rats by chronic treatment with hCG and insulin

Puberty and Ovarian Function in Girls with Type 1 Diabetes Mellitus

Obesity Management in Women with Polycystic Ovary Syndrome

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