Disease relevance of PCOS1

• Hyperandrogenism in polycystic ovary syndrome [1].
• Priming with human chorionic gonadotropin before retrieval of immature oocytes in women with infertility due to the polycystic ovary syndrome [2].
• BACKGROUND: Women with the polycystic ovary syndrome have insulin resistance and hyperinsulinemia, possibly because of a deficiency of a D-chiro-inositol-containing phosphoglycan that mediates the action of insulin [3].
• Detection of an alteration in the insulin-receptor gene in a patient with insulin resistance, acanthosis nigricans, and the polycystic ovary syndrome (type A insulin resistance) [4].
• These abnormalities, together with obesity, explain the substantially increased prevalence of glucose intolerance in PCOS [5].

Psychiatry related information on PCOS1

• METHODS: Three hundred women 18 to 45 years old with bipolar disorder were evaluated for PCOS at 16 Systematic Treatment Enhancement for Bipolar Disorder sites [6].
• Modifying additional lifestyle factors, including alcohol consumption, psychosocial stressors and smoking, are also crucial in long-term treatment of PCOS [7].
• Health-related quality of life measured with the 36-item short-form health survey revealed significantly decreased scores for physical role function, bodily pain, vitality, social function, emotional role function, and mental health in patients with PCOS [8].
• Menstrual abnormalities and polycystic ovary syndrome in women taking valproate for bipolar mood disorder [9].
• It is proposed that these closely interlinked phenomena that, particularly in overweight subjects, are associated with anovulation, may confer a biological advantage for women with PCOS at times of food deprivation, when such women may reproduce more successfully than those without PCOS [10].

High impact information on PCOS1

• In cortisone reductase deficiency (CRD), activation of cortisone to cortisol does not occur, resulting in adrenocorticotropin-mediated androgen excess and a phenotype resembling polycystic ovary syndrome (PCOS; refs. 1,2) [11].
• METHODS: We measured steroids in serum and performed oral glucose-tolerance tests before and after the oral administration of 1200 mg of D-chiro-inositol or placebo once daily for six to eight weeks in 44 obese women with the polycystic ovary syndrome [3].
• CONCLUSIONS: D-Chiro-inositol increases the action of insulin in patients with the polycystic ovary syndrome, thereby improving ovulatory function and decreasing serum androgen concentrations, blood pressure, and plasma triglyceride concentrations [3].
• Ovulatory and metabolic effects of D-chiro-inositol in the polycystic ovary syndrome [3].
• CONCLUSIONS: The ovulatory response to clomiphene can be increased in obese women with the polycystic ovary syndrome by decreasing insulin secretion with metformin [12].

Chemical compound and disease context of PCOS1

• CONCLUSIONS: In obese women with the polycystic ovary syndrome, decreasing serum insulin concentrations with metformin reduces ovarian cytochrome P450c17 alpha activity and ameliorates hyperandrogenism [13].
• Polycystic ovary syndrome as a form of functional ovarian hyperandrogenism due to dysregulation of androgen secretion [14].
• Recently introduced statistical tools capable of discerning differences between the pattern of luteinizing hormone (LH) secretion and that of follicle-stimulating hormone (FSH) could be valuable in understanding ovulation and menopause, and ultimately in making diagnostic decisions and treating infertility and polycystic ovary syndrome [15].
• 11 patients with polycystic ovary syndrome (hirsutism and oligomenorrhoea), but with no deficiency of 21-hydroxylase or 3 beta-hydroxysteroid dehydrogenase, had abnormal cortisol metabolism [16].
• Hormonally regulated serine phosphorylation of human P450c17 suggests a possible mechanism for human adrenarche and may be a unifying etiologic link between the hyperandrogenism and insulin resistance that characterize the polycystic ovary syndrome [17].

Biological context of PCOS1

• Effects of metformin on spontaneous and clomiphene-induced ovulation in the polycystic ovary syndrome [12].
• We compared 16 normal women in the follicular phase, 5 normal men, 8 women with polycystic ovary syndrome, and 1 woman with polycystic ovary syndrome caused by a 3 beta-hydroxysteroid dehydrogenase deficiency [18].
• Furthermore, there are less data to substantiate an increased risk of events in women with PCOS identified on the basis of a combination of signs and symptoms, such as hyperandrogenic chronic anovulation [19].
• Among others, genomic variants in genes related to the regulation of androgen biosynthesis and function, insulin resistance, and the metabolic syndrome, and proinflammatory genotypes may be involved in the genetic predisposition to functional hyperandrogenism and PCOS [20].
• The insulin resistance in at least 50% of PCOS women appears to be related to excessive serine phosphorylation of the insulin receptor [5].

Anatomical context of PCOS1

• Hyperandrogenemia is the hallmark of the polycystic ovary syndrome, yet the relative contributions of the adrenal cortex and ovary to the overproduction of androgen remain unclear [21].
• This finding points to the central nervous system as the probable locus of the initiating pathophysiology of polycystic-ovary syndrome [22].
• Approximately 50% of PCOS women (PCOS-Ser) had a significant increase in insulin-independent beta-subunit [32P]phosphate incorporation (3.7-fold, P < 0.05 vs other groups) in skin fibroblast insulin receptors that was present in serine residues while insulin-induced tyrosine phosphorylation was decreased (both P < 0.05 vs other groups) [23].
• PCOS skeletal muscle insulin receptors had the same abnormal phosphorylation pattern [23].
• We previously reported lower downstream resistance in the internal carotid artery in women with polycystic ovary syndrome [24].

Associations of PCOS1 with chemical compounds

• Decreases in ovarian cytochrome P450c17 alpha activity and serum free testosterone after reduction of insulin secretion in polycystic ovary syndrome [13].
• Abnormal luteinizing hormone secretion in polycystic-ovary syndrome [25].
• Patients with polycystic ovary syndrome responded to gonadotropin stimulation with normal to increased production of plasma estrogens and increased levels of androstenedione at 16 to 24 hours (P less than 0.05) [18].
• We measured 24-hour urinary excretion of steroid hormone metabolites by high-resolution capillary gas chromatography in 65 women with the polycystic ovary syndrome and 45 normal women matched for body-mass index [21].
• Adrenal secretion of cortisol and androgens is increased in women with the polycystic ovary syndrome [21].

Physical interactions of PCOS1

• BACKGROUND: Endocrine treatment of hyperandrogenism in women with polycystic ovary syndrome (PCOS) aims at reduction of androgens and increasing sex hormone binding globuline (SHBG), which are also side effects of ovarian electrocautery (OE) when used for induction of ovulation [26].

Regulatory relationships of PCOS1

• Alterations in mitogen-activated protein kinase kinase and extracellular regulated kinase signaling in theca cells contribute to excessive androgen production in polycystic ovary syndrome [27].
• Corticotropin-releasing hormone induces an exaggerated response of adrenocorticotropic hormone and cortisol in polycystic ovary syndrome [28].
• Are women with polycystic ovary syndrome resistant to activated protein C [29]?
• Combined somatostatin analog and follicle-stimulating hormone for women with polycystic ovary syndrome resistant to conventional treatment [30].
• Aromatase activity can be activated when granulosa are isolated from the polycystic ovary syndrome follicle but is not active in the follicle in situ [31].

Other interactions of PCOS1

• Upregulation of adiponectin receptor 1 and 2 mRNA and protein in adipose tissue and adipocytes in insulin-resistant women with polycystic ovary syndrome [32].
• SHBG levels are frequently low in women with polycystic ovary syndrome (PCOS) and may contribute to increased tissue exposure to free androgens [33].
• Lack of an association between peroxisome proliferator-activated receptor-gamma gene Pro12Ala polymorphism and adiponectin levels in the polycystic ovary syndrome [34].
• Follicular fluid insulin-like growth factor binding protein profiles in polycystic ovary syndrome [35].
• Relationship of insulin receptor substrate-1 and -2 genotypes to phenotypic features of polycystic ovary syndrome [36].

Analytical, diagnostic and therapeutic context of PCOS1

• METHODS: We performed oral glucose-tolerance tests before and after the administration of 500 mg of metformin or placebo three times daily for 35 days in 61 obese women with the polycystic ovary syndrome [12].
• Gynecologists, endocrinologists, cardiologists, pediatricians, and dermatologists are all concerned with PCOS patients and share research data and design clinical trials to learn more about the syndrome [37].
• Future studies to identify the risk of cardiovascular events in women with PCOS will benefit from clear and extensive phenotyping of PCOS abnormalities at baseline, from a prospective design, from larger sample sizes, and from longer follow-up [19].
• Epidemiological studies that have focused on isolated signs and stigmata of PCOS, such as polycystic ovaries, hyperandrogenism, or chronic anovulation, have found mixed results [19].
• The INS VNTR III/III genotype was associated with an increased risk of PCOS in two independent case-control studies (odds ratios 8.20 [p = 0.005] and 5.70 [p = 0.043]) [38].

References