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Hyperinsulinemia Hyperandrogenism

Polycystic Ovarian Syndrome (pcos)

Polycystic Ovarian Syndrome (pcos)

PCOS is characterized by hyperandrogenism, irregular ovulatory cycles, and a metabolic derangement including glucose intolerance and hyperinsulinemia. Manifestations of PCOS are heterogeneous, and several consensus definitions of the disorder have been produced to describe the disease, with various emphases on clinical or biochemical hyperandrogenism, polycystic ovaries, and oligoanovulation. The Rotterdam Consensus (2003) defines PCOS as at least two of the following characteristics: Clinical hyperandrogenism and/or hyperandrogenemia Oligoanovulation Polycystic ovaries on ultrasound Although other definitions emphasize the presence of clinical or biochemical hyperandrogenism as an important characteristic of the disease, there is some debate as to the centrality of hyperandrogenism in PCOS. The more inclusive Rotterdam criteria may be appropriate in patients where clinical hyperandrogenism is difficult to assess. Genetics: PCOS is believed to be a complex disorder, with genetic as well as environmental factors contributing to development of the disease. 20-40% of female first-degree relatives of women with PCOS also have the syndrome, suggesting that the disease is partially heritable and clusters in families. Prevalence and severity of presentation vary with ethnicity, with South Asians at a higher risk of disease. Some candidate genes have been identified as contributing to risk of the disease, including 7β-hydroxysteroid-dehydrogenase type 6 (HSD17B6). Intrauterine exposures: exposures to testosterone in utero may predispose to the later development of PCOS. Animal studies have demonstrated that in utero exposure is correlated with development of a PCOS-like syndrome including hyperinsulinemia, hyperandrogenism, oligoanovulation, and polycystic ovaries. Exposure to Continue reading >>

Sensitization To Insulin In Adolescent Girls To Normalize Hirsutism, Hyperandrogenism, Oligomenorrhea, Dyslipidemia, And Hyperinsulinism After Precocious Pubarche

Sensitization To Insulin In Adolescent Girls To Normalize Hirsutism, Hyperandrogenism, Oligomenorrhea, Dyslipidemia, And Hyperinsulinism After Precocious Pubarche

Precocious pubarche in girls is often preceded by low weight at birth and followed by hirsutism, ovarian hyperandrogenism, and oligomenorrhea in adolescence, the latter usually being accompanied by dyslipidemia and hyperinsulinism, which are, in turn, two major risk factors for cardiovascular disease in later life. We hypothesized that insulin resistance may be a key pathogenetic factor in this sequence. We tested the hypothesis by assessing the effects of an insulin-sensitizing agent, metformin, given at a daily dose of 1275 mg for 6 months to 10 nonobese adolescent girls (mean age, 16.8 yr; body mass index, 21.9 kg/m2; birth weight, 2.7 kg) with hirsutism, ovarian hyperandrogenism (diagnosis by GnRH agonist test), oligomenorrhea, dyslipidemia, and hyperinsulinemia after precocious pubarche. Before the metformin trial, longitudinal studies in these girls had shown that hyperinsulinism was present at prepubertal diagnosis of precocious pubarche, and that it increased markedly in late puberty or early postmenarche. Metformin treatment was well tolerated and was accompanied by a marked drop in hirsutism score, insulin response to oral glucose tolerance test, free androgen index, and baseline testosterone, androstenedione, dehydroepiandrosterone, and dehydroepiandrosterone sulfate levels (all P < 0.01). During metformin treatment, the LH and 17-hydroxyprogesterone hyperresponses to GnRH agonist were attenuated (P < 0.01); serum triglyceride, total cholesterol, and low density lipoprotein cholesterol levels decreased; and high density lipoprotein cholesterol rose. All girls reported regular menses within 4 months. Withdrawal of metformin treatment was followed, within 3 months, by a consistent reversal toward pretreatment conditions. In conclusion, metformin treatment redu Continue reading >>

Improvement Of Hyperandrogenism And Hyperinsulinemia During Pregnancy In Women With Polycystic Ovary Syndrome: Possible Effect In The Ovarian Follicular Mass Of Their Daughters - Sciencedirect

Improvement Of Hyperandrogenism And Hyperinsulinemia During Pregnancy In Women With Polycystic Ovary Syndrome: Possible Effect In The Ovarian Follicular Mass Of Their Daughters - Sciencedirect

Volume 97, Issue 1 , January 2012, Pages 218-224 Improvement of hyperandrogenism and hyperinsulinemia during pregnancy in women with polycystic ovary syndrome: possible effect in the ovarian follicular mass of their daughters Presented in part at the 91st Annual Meeting of the Endocrine Society, Washington DC, June 10, 2009. Get rights and content To evaluate the ovarian function during early infancy in daughters of women with polycystic ovary syndrome (PCOS) treated with metformin throughout pregnancy (PCOSd+M), as a means to reduce androgen and insulin levels, compared with daughters of nontreated PCOS women (PCOSdM) and daughters of women who belong to a healthy comparison group (HCd). Unit of endocrinology and reproductive medicine. Fifteen PCOSd+M, 23 PCOSdM, and 35 HCd were studied at 23 months of age. A GnRH analogue test was performed with determinations of gonadotropins, sex steroids, SHBG, and anti-Mllerian hormone (AMH). Differences in AMH levels between PCOSd+M, PCOSdM and HCd. AMH and peak E2 concentrations were significantly higher in PCOSdM compared with HCd, whereas PCOSd+M exhibited AMH concentrations and peak E2 levels similar to those observed in HCd. The improvement of the altered endocrine-metabolic environment of PCOS mothers reduces AMH levels in their daughters, which might reflect a decrease in their follicular mass. Choose an option to locate/access this article: Check if you have access through your login credentials or your institution. N.C. has nothing to disclose. B.E. has nothing to disclose. M.M. has nothing to disclose. V.P. has nothing to disclose. A.L.d.G. has nothing to disclose. J.P. has nothing to disclose. F.S has nothing to disclose. T.S.-P. has nothing to disclose. Supported by Fondo Nacional de Desarrollo Cientfico y Tecnolgico Continue reading >>

Hyperinsulinemia In Polycystic Ovary Syndrome: Relationship To Clinical And Hormonal Factors

Hyperinsulinemia In Polycystic Ovary Syndrome: Relationship To Clinical And Hormonal Factors

, Volume 72, Issue11 , pp 853857 | Cite as Hyperinsulinemia in polycystic ovary syndrome: relationship to clinical and hormonal factors We analyzed the association between hyperandrogenism and hyperinsulinemia, and their relationship to body mass index, in a large series of patients with polycystic ovary syndrome (PCOS). A characteristic hormonal profile was sought in women with marked hyperinsulinemia. The patient group consisted of 73 women with PCOS, ranging in age from 16 to 29 years. The control group consisted of 34 healthy women with no evidence of hyperandrogenism, aged 1930 years. None of the patients or control women had a body mass index above 27 kg/m2. Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, estradiol, androstenedione, dehydroepiandrosterone sulfate, sex hormone binding globulin, 17-hydroxyprogesterone, and free cortisol were determined by radioimmunoassay. The free testosterone index was calculated. The oral glucose tolerance test was used to analyze basal insulinemia, maximum insulin peak, and the insulinemia/glycemia index. In the group with PCOS body mass index was greater, free testosterone index was higher, and levels of dehydroepiandrosterone sulfate, testosterone, 17-hydroxyprogesterone (P < 0.001) and androstenedione (P < 0.05) were higher than in the control group. Of the insulin parameters, basal insulinemia, maximum insulin peak, and insulinemia/glycemia index were higher in the patient group (P < 0.001). In patients with marked insulinemia, free testosterone index was more markedly elevated, and gonadotrophin levels were normal. Our data confirm that a characteristic pattern of hyperinsulinemia is associated with PCOS. We found no causal relationship between hyperinsulinemia and androgen levels. A characteris Continue reading >>

Hyperandrogenism - Wikipedia

Hyperandrogenism - Wikipedia

Testosterone is a type of androgen that is important in the development of hyperandrogenism since high levels of it can cause this condition. Hyperandrogenism, also known as androgen excess, is a medical condition characterized by excessive levels of androgens (male sex hormones such as testosterone) in the female body and the associated effects of the elevated androgen levels. It is an endocrinological disorder similar to hyperestrogenism . The most common conditions associated with hyperandrogenism are polycystic ovary syndrome or PCOS, a set of symptoms caused by androgen excess in females, and various cancers that can cause androgen excess. In females, the conditions usually present are some combination of acne , seborrhea (inflamed skin), hair loss on the scalp, increased body and/or facial hair ( hirsutism ), and an elevated sex drive or libido . The symptoms of hyperandrogenism are usually most effectively treated with antiandrogens . There is some controversy over whether hyperandrogenism provides an unfair advantage in athletics. A person with hirsutism from increased androgen exposure Hyperandrogenism affects 5-10% of females of reproductive age. [1] Hyperandrogenism can affect both males and females, but is more noticeable in females due to the fact that elevated levels of androgens in females often facilitates virilization . Due to the fact that hyperandrogenism is characterized by the elevation of male sex hormone levels, symptoms of hyperandrogenism in men are often negligible. Hyperandrogenism in females is typically diagnosed in late adolescence with a medical evaluation. The medical evaluation tends to consist of a pelvic exam, observation of external symptoms, and a blood test measuring androgen levels. [2] Hyperandrogenism, especially high levels of Continue reading >>

Hyperandrogenism And Hyperinsulinemia

Hyperandrogenism And Hyperinsulinemia

INTRODUCTION Hyperinsulinemia and hyperandrogenism represent a tangled web that reaches its greatest complexity in women with polycystic ovary syndrome (PCOS). Researchers are beginning to separate the strands of the relationship between the two, but the pattern is still not clear. Initial data seem to suggest that the hyperinsulinemia, rather than the hyperandrogenemia, holds perhaps the gravest implications for long-term complications of the syndrome, such as cardiovascular disease and development of non - insulin-dependent diabetes mellitus (NIDDM). But the data supporting these long-term complications in women with PCOS are still scant. As gynecologists, we have traditionally focused on the hyperandrogenic aspects of this syndrome: hirsutism, dysfunctional uterine bleeding, and infertility. But as we identify the long-term sequelae, our primary concern for these patients may become improving insulin sensitivity. Because they frequently develop symptoms at the time of menarche, they represent an ideal target group for early intervention. This chapter will focus mainly on insulin resistance in PCOS, but other causes of hyperandrogenism and hyperinsulinemia also will be discussed. INSULIN RESISTANCE Insulin is the primary glucoregulatory hormone and is secreted by the beta cells of the pancreas. Its primary target tissues are skeletal muscle, liver, and adipose tissue. Of these, skeletal muscle is the largest target for insulin action. In the liver, insulin promotes glycogen formation and inhibits gluconeogenesis and glycogenolysis. In fat and muscle, insulin promotes glucose utilization and storage. Insulin is a potent growth factor, and its effects on peripheral tissues are pleiotropic and potentially not all favorable. In high doses, it may be directly atherogenic o Continue reading >>

Insulin And Hyperandrogenism In Women With Polycystic Ovary Syndrome

Insulin And Hyperandrogenism In Women With Polycystic Ovary Syndrome

Insulin and hyperandrogenism in women with polycystic ovary syndrome Department of Medicine, Division of Endocrinology, University of Sherbrooke, 3001 12th North Avenue, Sherbrooke, QC J1H 5N4, Canada *Corresponding author. Tel.: +1 819 346 1110x14853; fax: +1 819 564 5292. [email protected] (J.-P. Baillargeon) The publisher's final edited version of this article is available at J Steroid Biochem Mol Biol See other articles in PMC that cite the published article. Polycystic ovary syndrome (PCOS) is a very common endocrine disorder characterized by chronic anovulation, clinical and/or biochemical hyperandrogenism, and/or polycystic ovaries. But most experts consider that hyperandrogenism is the main characteristic of PCOS. Several theories propose different mechanisms to explain PCOS manifestations: (1) a primary enzymatic default in the ovarian and/or adrenal steroidogenesis; (2) an impairment in gonadotropin releasing hormone (GnRH) secretion that promotes luteal hormone (LH) secretion; or (3) alterations in insulin actions that lead to insulin resistance with compensatory hyperinsulinemia. However, in the past 20 years there has been growing evidence supporting that defects in insulin actions or in the insulin signalling pathways are central in the pathogenesis of the syndrome. Indeed, most women with PCOS are metabolically insulin resistant, in part due to genetic predisposition and in part secondary to obesity. But some women with typical PCOS do not display insulin resistance, which supports the hypothesis of a genetic predisposition specific to PCOS that would be revealed by the development of insulin resistance and compensatory hyperinsulinemia in most, but not all, women with PCOS. However, these hypotheses are not yet appropriately confirmed, and m Continue reading >>

Hyperinsulinism And Its Interaction With Hyperandrogenism In Polycystic Ovary Syndrome

Hyperinsulinism And Its Interaction With Hyperandrogenism In Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. It has become increasingly evident that insulin resistance plays a significant role both as a cause and result of the syndrome. The purpose of this review is to summarize the possible mechanisms leading to insulin resistance and resultant hyperinsulinism (HI) and their interaction with hyperandrogenism (HA) in PCOS. We conducted a computerized search of MEDLINE for relevant studies in the English literature published between January 1966 and January 2000. We reviewed all studies that investigated the roles of insulin, insulin receptor, and insulin gene in insulin resistance and its interaction with hyperandrogenism in PCOS. Insulin resistance in PCOS seems to involve a postbinding defect in the insulin receptor and/or in the receptor signal transduction. Current research has focused on identifying a genetic predisposition for insulin resistance in this syndrome. The answer to the question whether HI or HA is the initiating event is still unclear inasmuch as there are clinical and molecular evidences to support both of these approaches. Our view is that whichever is the triggering insult, a vicious cycle is established where HI acts to aggravate HA and vice versa. In this model, obesity and genetic predisposition seem to be the independent factors that can give rise or contribute to HI, HA, or both simultaneously. It seems that hyperinsulinemic hyperandrogenism represents a significant subgroup of PCOS, which probably needs to be renamed and reclassified in the light of this new approach. Target AudienceObstetricians & Gynecologists, Family Physicians Learning ObjectivesAfter completion of this article, the reader will be able to summarize the possible mechanisms leading Continue reading >>

Hyperandrogenism And Skin: Polycystic Ovary Syndrome And Peripheral Insulin Resistance

Hyperandrogenism And Skin: Polycystic Ovary Syndrome And Peripheral Insulin Resistance

REVIEW ARTICLE Samira YarakI; Ediléia BagatinII; Karime Marques HassunIII; Meire Odete Américo Brasil ParadaIV; Sérgio Talarico FilhoV Universidade Federal de São Paulo - Escola Paulista de Medicina (Unifesp-EPM) - São Paulo (SP), Brazil - Department of Dermatology ICommissioned physician. Master's degree in Dermatology IIPhysician. Ph.D. degree in Dermatology IIIPhysician. Master's degree in Dermatology IVVolunteer physician VAdjunct Professor, Master's degree in Dermatology ABSTRACT The polycystic ovary syndrome is an extremely common endocrine disorder in women of chilbearing age. It is characterized by menstrual disturbance, hyperandrogenism and/or hyperandrogenemia. The primary pathophysiological defect is unknown, but important characteristics include insulin resistance, androgen excess and impaired gonadotropin dynamics. The most frequent clinical characteristics of polycystic ovary syndrome are associated with the pilosebaceous unit, such as hirsutism, acne, seborrhea and alopecia. Thus, the dermatologist may be responsible for making an early diagnosis of the syndrome, thus preventing delay in establishing preventive and therapeutic measures. The current management recommended for skin manifestations of polycystic ovary syndrome includes combined oral contraceptives, antiandrogens and insulin-sensitizing agents, besides changes in life style. This is a review article on diagnosis, pathophysiology and treatment of polycystic ovary syndrome. The authors emphasize that a clear understanding of pathophysiology of this syndrome, especially by dermatologists, is crucial for its preventive treatment through the different phases in the life of women. Keywords: Hyperandrogenism / diagnosis; Hyperandrogenism / therapy; Skin; Insulin resistance; Hypothalamic-pituitar Continue reading >>

Polycystic Ovary Syndrome (pcos)

Polycystic Ovary Syndrome (pcos)

We list the most important complications. The selection is not exhaustive. 1. Azziz R. Epidemiology and pathogenesis of the polycystic ovary syndrome in adults. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. . Last updated August 24, 2015. Accessed March 15, 2017. 2. Jenkins B, McInnis M, Lewis C. Step-Up to USMLE Step 2 CK. Lippincott Williams & Wilkins; 2015. 3. Comninos AN, Jayasena CN, Dhillo WS. The relationship between gut and adipose hormones, and reproduction. Hum Reprod Update. 2013; 20(2): pp.153174. doi: 10.1093/humupd/dmt033 . 4. Master-Hunter T, Heiman DL. Amenorrhea: Evaluation and Treatment. Am Fam Physician. 2006; 73(8): pp.13741382. url: . 5. Lucidi RS. Polycystic Ovarian Syndrome. In: Polycystic Ovarian Syndrome. New York, NY: WebMD. . Updated August 11, 2016. Accessed February 17, 2017. 6. Eunice Kennedy Shriver National Institute of Child Health and Human Development. What causes amenorrhea?. . Updated March 15, 2017. Accessed March 15, 2017. 7. Rosenfield RL. Definition, clinical features and differential diagnosis of polycystic ovary syndrome in adolescents. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. . Last updated February 10, 2017. Accessed March 15, 2017. 8. Goodman NF, Cobin RH, Futterweit W, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and Androgen Excess and PCOS Society Disease State Clinical Review: Guide to the best Practices in the Evaluation and Treatment of Polycystic Ovary Syndrome: Part 1. Endocr Pract. 2015; 21(11): pp.12911300. doi: 10.4158/EP15748.DSC . 9. Sterling E. Hormone Levels and PCOS. . Updated November 7, 2015. Accessed February 17, 2017. 10. Barbieri RL, Ehrmann DA. Diagnosis of polycystic ovary syndrome in adults. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Continue reading >>

Hyperandrogenism And Insulin Resistance

Hyperandrogenism And Insulin Resistance

The association between hyperandrogenism and insulin resistance in women has been known since 1921 [1]. This so-called Archard-Thiers syndrome has also been referred to as diabetes of bearded women. Although these original findings were repeatedly observed [25], the cause and effect relationship between hyperandrogenism and hyperinsulinemia has not been clearly delineated. The current literature on the pathophysiology of hyperandrogenism-insulin resistance and the clinical implications of this association are reviewed below. Insulin ResistanceInsulin ReceptorPolycystic Ovary SyndromeCongenital Adrenal HyperplasiaAcanthosis Nigricans These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Archard C, Thiers J (1921) Le virilisme pilaire et son association a linsuffisance glycolytique (diabete a femmes de barbe). Bull Acad Natl Med (Paris) 86:51 Google Scholar Barbieri RL, Ryan KJ (1983) Hyperandrogenism, insulin resistance and acanthosis nigricans syndrome: a common endocrinopathy and distinct pathophysiologic features. Am J Obstet Gynecol 147:90 PubMed Google Scholar Chang RJ, Geffner ME (1985) Associated non-ovarian problems of polycystic ovarian disease: insulin resistance. Clin Obstet Gynaecol 12:675 PubMed Google Scholar Poretsky L, Kalin MF (1987) The gonadotropic function of insulin. Endocr Rev 8:132 PubMed CrossRef Google Scholar Barbieri RL, Smith S, Ryan KJ (1988) The role of hyperinsulinemia in the pathogenesis of ovarian hyperandrogenism. Fertil Steril 50:197 PubMed Google Scholar Krauth MC, Schillinger E (1977) Changes in insulin receptor concen Continue reading >>

Polycystic Ovary Syndrome

Polycystic Ovary Syndrome

J Midwifery Womens Health.2006;51(6):415-422. A complete understanding of the underlying pathophysiology of PCOS is still lacking. Because of the heterogeneity of this disorder, there are most likely multiple underlying pathophysiologic mechanisms. Several theories have been proposed to explain the pathogenesis of PCOS.[ 8 ] 1) An alteration in gonadotropin-releasing hormone secretion results in increased luteinizing hormone (LH) secretion. 2) An alteration in insulin secretion and insulin action results in hyperinsulinemia and insulin resistance. 3) A defect in androgen synthesis that results in increased ovarian androgen production. We will discuss each of these theories in more detail. LH hypersecretion is a characteristic hallmark of PCOS. LH is secreted in a pulsatile manner. Women with PCOS have an increase in both the LH pulse frequency and amplitude, resulting in increased 24-hour secretion. This increase in LH secretion is thought to occur as a result of increased frequency of hypothalamic gonadotropin-releasing hormone (GnRH) pulses. Increased LH, in turn, leads to an increase in androgen production by the theca cells within the ovary.[ 3 , 8 ] Insulin resistance, defined as reduced glucose response to a given amount of insulin, is a characteristic metabolic disturbance associated with PCOS. Both obese and nonobese women with PCOS have a higher incidence of insulin resistance and hyperinsulinemia than age-matched controls; however, obese women with PCOS have significantly decreased insulin sensitivity compared with nonobese women who have PCOS. Insulin resistance is known to precede the development of type 2 diabetes mellitus. Studies have shown that 30% to 40% of women with PCOS have impaired glucose tolerance, and as many as 10% develop type 2 diabetes mell Continue reading >>

The Role Of Hyperinsulinemia In The Pathogenesis Of Ovarian Hyperandrogenism.

The Role Of Hyperinsulinemia In The Pathogenesis Of Ovarian Hyperandrogenism.

The role of hyperinsulinemia in the pathogenesis of ovarian hyperandrogenism. Department of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, Massachusetts. The evidence that supports the hypothesis that insulin and LH both regulate ovarian androgen production was presented. The most dramatic clinical example of the association between hyperinsulinemia and hyperandrogenism is the HAIR-AN syndrome. Our hypothesis is that, in the HAIR-AN syndrome, the severe insulin resistance causes a compensatory hyperinsulinemia, which stimulates ovarian androgen production if adequate LH is present. The acanthosis nigricans is an epiphenomenon of the syndrome. Acanthosis nigricans is a dermatologic manifestation of severe insulin resistance. In vitro evidence suggests that insulin and IGF-I stimulate androgen production in incubations of human stroma and theca. The stromatropic effects of insulin may sensitize the stroma to the stimulatory effects of LH. In some hyperandrogenic-insulin-resistant women, a glucose load appears to produce an acute rise in circulating androgens. The magnitude of the rise in circulating androgens is proportional to the magnitude of the insulin response to the glucose load. These data suggest that hyperinsulinemia may play a central role in the development of ovarian hyperandrogenism. Continue reading >>

Hyperandrogenism, Insulin Resistance And Hyperinsulinemia As Cardiovascular Risk Factors In Diabetes Mellitus

Hyperandrogenism, Insulin Resistance And Hyperinsulinemia As Cardiovascular Risk Factors In Diabetes Mellitus

Hyperandrogenism, Insulin Resistance and Hyperinsulinemia as Cardiovascular Risk Factors in Diabetes Mellitus Author(s): Gema Garcia-Romero , Hector F. Escobar-Morreale . Department of Endocrinology, Hospital Ramn y Cajal. Carretera de Colmenar Km 9,100. 28034 Madrid, Spain. The polycystic ovary syndrome (PCOS) and hyperandrogenism are some of the most common endocrine disorders in women of fertile age. Insulin resistance is present in a significant proportion of hyperandrogenic patients, yet also, impaired -cell function, even in absence of clinically evident glucose intolerance, is a frequent finding, especially in patients with familial history of type 2 diabetes mellitus. Therefore, it is not surprising that hyperandrogenism, PCOS, and disorders of carbohydrate metabolism are associated frequently. This association was first reported 75 years ago and, although the mechanisms responsible are not precisely understood, insulin resistance plays an important role in the development of both disorders. PCOS patients develop type 2 diabetes mellitus more frequently than non-hyperandrogenic women and, conversely, women with type 2 diabetes have a greater risk of having PCOS compared with the normal population. Although type 1 diabetes mellitus is a disease characterized by complete abolition of endogenous insulin secretion, a certain degree of hyperinsulinism may exist, resulting from the relatively excessive insulin doses needed to maintain a strict metabolic control. This exogenous hyperinsulinism may increase ovarian androgen secretion, and it has been reported that there is an increased prevalence of hyperandrogenic disorders in type 1 diabetic women. Considering that insulin resistance, hyperinsulinemia and androgen excess may collaborate in increasing the risk for CVD Continue reading >>

Polycystic Ovary Syndrome

Polycystic Ovary Syndrome

Description Polycystic ovary syndrome (PCOS) is the most common cause of anovulatory infertility. Its prevalence among women of reproductive age is estimated to be between 5-10%. PCOS is classified as a syndrome because it is a heterogeneous disorder: not all of the women with PCOS will express all of the symptoms associated with the disorder. A diagnosis of PCOS is made if a woman has chronic problems with ovulation coupled with hyperandrogenism (excess secretion of androgens). Problems with ovulation will manifest themselves as amenorrhea (lack of menstruation) or oligomenorrhea (irregular menstruation). Hyperandrogenism may cause hirsutism, which is a masculine pattern of hair growth on the body, and acne, because androgens have an effect on the sebaceous glands of the skin that promotes acne. Androgens may also cause hair loss on the scalp. PCOS gets its name from the changes seen in the ovary (although not all women with PCOS have polycystic ovaries). Polycystic ovaries are enlarged and contain multiple (greater than 10) immature follicles. The immature follicles show a relative hyperplasia of theca cells, and fewer granulosa cells. Development of these follicles is arrested well before the point of dominant follicle selection, so the LH surge doesn't occur, and therefore, neither does ovulation. There are also metabolic disturbances associated with PCOS. Frequently, women with PCOS are found to be insulin resistant. Because insulin resistance is a decreased sensitivity to insulin, this means that more insulin is necessary to achieve the same effect. For this reason, individuals who are insulin resistant have higher levels of insulin secretion or hyperinsulinemia. Because women with PCOS are insulin resistant, they are at a greater risk for developing type 2 diabet Continue reading >>

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