scholarly journals MON-213 Evaluation of Type 2 Diabetes and Cardiovascular Disease Risk Factors in Reproductive-Age Women with Polycystic Ovary Syndrome (PCOS) Using the 2014 Androgen Excess and PCOS Society Criteria for the Polycystic Ovarian Morphology

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Maryam Kazemi ◽  
Roger Pierson ◽  
Marla Lujan ◽  
Philip Chilibeck ◽  
Laura McBreairty ◽  
...  
Keyword(s):  
Risk Factors ◽  
Disease Risk ◽  
Polycystic Ovary ◽  
Cardiovascular Disease Risk ◽  
Reproductive Age ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Reproductive Age Women ◽  
Ovarian Morphology

scholarly journals Analysis of the vascular responses in a murine model of polycystic ovary syndrome

2013 ◽  
Vol 218 (2) ◽  
pp. 205-213 ◽  
Author(s):  
Sieneke Labruijere ◽  
E Leonie A F van Houten ◽  
René de Vries ◽  
Usha M Musterd-Bagghoe ◽  
Ingrid M Garrelds ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Polycystic Ovary Syndrome ◽  
Vascular Function ◽  
Disease Risk ◽  
Polycystic Ovary ◽  
Cardiovascular Disease Risk ◽  
Endothelial Damage ◽  
Reproductive Age ◽  
Enos Expression ◽  
Ovary Syndrome

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of the reproductive age, but the exact pathophysiological mechanisms involved remain unclear. Cardiovascular disease risk is increased in PCOS patients and endothelial damage has been observed. We recently developed a mouse model of PCOS with reproductive and metabolic characteristics resembling those observed in women with PCOS. In this model we studied vascular function with particular emphasis on markers of vascular endothelial function. Animals were treated for 90 days with dihydrotestosterone (DHT; 27.5 μg/day) or placebo using subcutaneous continuous-release pellets. Aortas were isolated for isometric force recordings in organ baths to investigate endothelial and vascular smooth muscle characteristics. Lungs were used to analyze endothelial nitric oxide synthase (eNOS) expression and phosphorylation. Asymmetric dimethylarginine (ADMA) levels were investigated in serum to assess endothelial damage. Expression of androgen receptor (Ar) mRNA was studied in aortas. DHT treatment (compared with placebo) induced i) a significant decrease in acetylcholine-induced aortic relaxations, with no change in calcitonin gene-related peptide- or sodium nitroprusside-induced relaxations, as well as 5-hydroxytryptamine-induced contractions; ii) no change in eNOS expression/phosphorylation in lungs or in plasma ADMA levels; and iii) a twofold increase in aortic AR expression. Our results suggest that, in DHT-exposed mice, hyperandrogenemia specifically decreases endothelium-dependent vasorelaxation without deterioration of smooth muscle function. This study may initiate further investigations to elucidate underlying mechanism for the phenotype that is present in these animals, as well as in PCOS patients.

scholarly journals Cardiometabolic Features of Polycystic Ovary Syndrome: Role of Androgens

Physiology ◽  
2017 ◽  
Vol 32 (5) ◽  
pp. 357-366 ◽  
Author(s):  
Licy L. Yanes Cardozo ◽  
Damian G. Romero ◽  
Jane F. Reckelhoff
Keyword(s):  
Risk Factors ◽  
Polycystic Ovary Syndrome ◽  
Cardiometabolic Risk ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Endocrine Disorder ◽  
Reproductive Age Women ◽  
Cardiometabolic Profile

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder that affects reproductive-age women. Hyperandrogenemia is present in a significant fraction (~80%) of women with PCOS. Increased prevalence of cardiometabolic risk factors is frequently observed in PCOS women. The present review aims to highlight the key role of androgens in mediating the negative cardiometabolic profile observed in PCOS women.

scholarly journals Inositols’ Importance in the Improvement of the Endocrine–Metabolic Profile in PCOS

2019 ◽  
Vol 20 (22) ◽  
pp. 5787 ◽  
Author(s):  
Anna Wojciechowska ◽  
Adam Osowski ◽  
Marcin Jóźwik ◽  
Ryszard Górecki ◽  
Andrzej Rynkiewicz ◽  
...  
Keyword(s):  
Metabolic Disorders ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Physiological Properties ◽  
Ovarian Morphology ◽  
Common Causes ◽  
Symptom Formation

Polycystic ovary syndrome (PCOS) is one of the most common causes of infertility and metabolic problems among women of reproductive age. The mechanism of PCOS is associated with concurrent alterations at the hormonal level. The diagnosis assumes the occurrence of three interrelated symptoms of varying severity, namely ovulation disorders, androgen excess, or polycystic ovarian morphology (PCOM), which all require a proper therapeutic approach. The main symptom seems to be an increased androgen concentration, which in turn may contribute to different metabolic disorders. A number of papers have demonstrated the significant role of inositol therapy in PCOS. However, there is a lack of detailed discussion about the importance of myo-inositol (MI) and d-chiro-inositol (DCI) in reference to particular symptoms. Thus, the aim of this review is to present the effectiveness of MI and DCI treatment for PCOS symptoms. Moreover, the review is focused on analyzing the use of inositols, taking into account their physiological properties, together with the mechanism of individual PCOS symptom formation.

scholarly journals Lipid-induced mononuclear cell cytokine secretion in the development of metabolic aberration and androgen excess in polycystic ovary syndrome

2020 ◽  
Vol 35 (5) ◽  
pp. 1168-1177
Author(s):  
F González ◽  
R V Considine ◽  
O A Abdelhadi ◽  
A J Acton
Keyword(s):  
Insulin Sensitivity ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Saturated Fat ◽  
National Institutes Of Health ◽  
Reproductive Age ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
Reproductive Age Women ◽  
Androgen Secretion

Abstract STUDY QUESTION What is the effect of saturated fat ingestion on mononuclear cell (MNC) TNFα, IL-6 and IL-1β secretion and circulating IL-6 levels in women with polycystic ovary syndrome (PCOS)? SUMMARY ANSWER Women with PCOS exhibit increases in MNC-derived TNFα, IL-6 and IL-1β secretion and circulating IL-6 following saturated fat ingestion even in the absence of obesity, and these increases are linked to metabolic aberration and androgen excess. WHAT IS KNOWN ALREADY Cytokine excess and metabolic aberration is often present in PCOS. STUDY DESIGN, SIZE, DURATION A cross-sectional design was used in this study of 38 reproductive-age women. PARTICIPANTS/MATERIALS, SETTING, METHODS Groups of 19 reproductive-age women with PCOS (10 lean, 9 obese) and 19 ovulatory controls (10 lean, 9 obese) participated in this study that was performed at a tertiary academic medical centre. TNFα, IL-6 and IL-1β secretion was measured from cultured MNC, and IL-6 was measured in plasma from blood sampling while fasting and 2, 3 and 5 h after saturated fat ingestion. Insulin sensitivity was determined using the Matsuda index following an oral glucose tolerance test. Androgen secretion was evaluated with blood sampling while fasting and 24, 48 and 72 h after an HCG injection. MAIN RESULTS AND THE ROLE OF CHANCE Lean and obese women with PCOS exhibited lipid-induced incremental AUC increases in MNC-derived TNFα (489–611%), IL-6 (333–398%) and IL-1β (560–695%) secretion and in plasma IL-6 levels (426–474%), in contrast with lean control subjects. In both PCOS groups, insulin sensitivity was lower (42–49%) and androgen secretion after HCG injection was greater (63–110%) compared with control subjects. The MNC-derived TNFα, IL-6 and IL-1β and circulating IL-6 responses were inversely associated with insulin sensitivity and directly associated with fasting lipids and androgen secretion after HCG injection. LIMITATIONS, REASONS FOR CAUTION The sample size of each of the four study groups was modest following group assignment of subjects by body mass. WIDER IMPLICATIONS OF THE FINDINGS This study showcases the unique pro-inflammatory contribution of circulating MNC in the development of metabolic aberration and androgen excess in PCOS. STUDY FUNDING/COMPETING INTEREST(S) This research was supported by grant R01 DK107605 to F.G. from the National Institutes of Health, the Indiana Clinical and Translational Sciences Institute Clinical Research Center which is funded in part by grant UL1TR002529 from the National Institutes of Health, National Center for Advancing Translational Sciences, Clinical and Translational Sciences Award, and the Indiana University Center for Diabetes and Metabolic Diseases funded by grant P30 DK097512 from the National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. No conflicts of interest, financial or otherwise, are declared by the authors. TRIAL REGISTRATION NUMBER ClinicalTrials.gov NCT01489319

scholarly journals Adiponectin and Polycystic Ovary Syndrome

2010 ◽  
Vol 12 (1) ◽  
pp. 62-72 ◽  
Author(s):  
Susan W. Groth
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Clinical Practice ◽  
Polycystic Ovary Syndrome ◽  
Disease Risk ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Increased Risk

Introduction. Polycystic ovary syndrome (PCOS) has a prevalence of 5—8% in women of reproductive age. Women with PCOS have an increased risk of metabolic syndrome and associated comorbidities. Adiponectin is a circulating protein produced by adipocytes. Circulating levels of adiponectin are inversely related to adipocyte mass. Low levels occur with insulin resistance, type 2 diabetes, metabolic syndrome, and obesity-related cardiovascular disease. This article reviews the literature on the link between adiponectin and PCOS and the potential use of adiponectin as a biomarker for PCOS. Method. Data-based studies on adiponectin and PCOS and adiponectin measurement were identified through the Medline (1950—2009) and ISI Web of Knowledge (1973—2009) databases. Results. Fifteen studies related to adiponectin and PCOS met inclusion criteria and were included in this review. These studies present evidence that adiponectin is linked to insulin resistance, insulin sensitivity, body mass index (BMI), and adiposity. In women with PCOS, lower levels, as opposed to higher levels, of adiponectin occur in the absence of adiposity. Conclusion. The relationships between adiponectin and insulin resistance and sensitivity, metabolic syndrome, and BMI in women with PCOS suggest that adiponectin potentially could serve as a marker for disease risk and provide opportunity for earlier intervention if knowledge is successfully translated from laboratory to clinical practice. However, further study of the relationship between adiponectin and PCOS is required before there can be direct application to clinical practice.

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