scholarly journals COMPARISONS OF GLUCOSE INTOLERANCE TESTING FOR THE DETECTION AND DIAGNOSIS OF PREDIABETES AND TYPE II DIABETES MELLITUS IN REPRODUCTIVE AGE WOMEN WITH POLYCYSTIC OVARY SYNDROME

2020 ◽  
Vol 114 (3) ◽  
pp. e404
Author(s):  
J. Ricardo Loret de Mola ◽  
Pamela Bremer ◽  
Teresa S. Wilson ◽  
Emma V. James ◽  
Kristin Delfino ◽  
...  
Diabetologia ◽  
2002 ◽  
Vol 45 (7) ◽  
pp. 959-964 ◽  
Author(s):  
T. Sir-Petermann ◽  
B. Angel ◽  
M. Maliqueo ◽  
F. Carvajal ◽  
J. Santos ◽  
...  

Physiology ◽  
2017 ◽  
Vol 32 (5) ◽  
pp. 357-366 ◽  
Author(s):  
Licy L. Yanes Cardozo ◽  
Damian G. Romero ◽  
Jane F. Reckelhoff

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.


MedPharmRes ◽  
2019 ◽  
Vol 2 (4) ◽  
pp. 26-31
Author(s):  
Chau Tran ◽  
Lan Vuong

Polycystic ovary syndrome (PCOS) is a common endocrine metabolic disorder in women of reproductive age. PCOS is often associated with insulin resistance and carries an increased risk of gestational diabetes mellitus (GDM). The aim of this study was to evaluate the risk of GDM in women with a history of PCOS. This was a retrospective cohort study conducted at a single center in Vietnam between January 2014 and December 2017. A total of 400 women who conceived through assisted reproductive technology (ART) were included, 200 who had been diagnosed with PCOS, and 200 without a PCOS diagnosis as controls. Multivariable logistic regression models were used to examine the association between risk of GDM and PCOS after adjusting for confounders. GDM was present in 37% of those with PCOS, compared with 26.5% in those without PCOS (RR 1.4, 95% CI 1.04–1.87, p=0.02). The prevalence of GDM did not differ significantly between PCOS phenotype groups (p=0.28). Women with PCOS undergoing ART had a higher risk of GDM after adjusting for differences in age, pre-pregnancy body mass index, type of infertility, ART indications, and type of ART (adjusted OR 2.04, 95% CI 1.06–3.92). First-trimester fasting plasma glucose (FPG) was also an independent predictor for GDM (adjusted OR 1.54, 95% CI 1.01–2.34). This study suggests that PCOS and first-trimester FPG are independent risk factors for the development of GDM.


2021 ◽  
pp. 097206342110115
Author(s):  
Gauri Pathak

Polycystic ovary syndrome (PCOS) is a hormonal disorder associated with increased risks of type II diabetes and cardiovascular disease. It is also the leading cause of female infertility worldwide. Both lifestyle and genetic factors have been tied to the condition, and in the last couple of decades, it has been affecting a growing number of urban Indian middle-class women; whereas global prevalence is in the 4–11% range, studies in India suggest a prevalence of around one in four urban middle-class women. In this article, I focus on the lived experiences of women with the condition. Drawing from ethnographic fieldwork in Mumbai, India, I use an ecosocial approach to examine barriers to the management of PCOS commonly experienced by women. Such an examination reveals potential bases for intervention to improve management outcomes, particularly as they relate to strengthening the patient–practitioner relationship and improving the clinical encounter.


2020 ◽  
Vol 35 (5) ◽  
pp. 1168-1177
Author(s):  
F González ◽  
R V Considine ◽  
O A Abdelhadi ◽  
A J Acton

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


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