Search Results
You are looking at 41 - 50 of 470 items for
- Abstract: adrenarche x
- Abstract: amenorrhoea x
- Abstract: fertility x
- Abstract: Gender x
- Abstract: Hypogonadism x
- Abstract: infertility x
- Abstract: Kallmann x
- Abstract: Klinefelter x
- Abstract: menopause x
- Abstract: puberty x
- Abstract: testes x
- Abstract: transsexual x
- Abstract: Turner x
- Abstract: sperm* x
- Abstract: ovary x
Search for other papers by Angela Köninger in
Google Scholar
PubMed
Search for other papers by Philippos Edimiris in
Google Scholar
PubMed
Search for other papers by Laura Koch in
Google Scholar
PubMed
Search for other papers by Antje Enekwe in
Google Scholar
PubMed
Search for other papers by Claudia Lamina in
Google Scholar
PubMed
Search for other papers by Sabine Kasimir-Bauer in
Google Scholar
PubMed
Search for other papers by Rainer Kimmig in
Google Scholar
PubMed
Department of Gynecology and Obstetrics, Division of Genetic Epidemiology, Vitateq Biotechnology GmbH, University of Duisburg-Essen, D-45122 Essen, Germany
Search for other papers by Hans Dieplinger in
Google Scholar
PubMed
Oxidative stress seems to be present in patients with polycystic ovary syndrome (PCOS). The aim of this study was to evaluate the correlation between characteristics of PCOS and serum concentrations of afamin, a novel binding protein for the antioxidant vitamin E. A total of 85 patients with PCOS and 76 control subjects were investigated in a pilot cross-sectional study design between 2009 and 2013 in the University Hospital of Essen, Germany. Patients with PCOS were diagnosed according to the Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group. Afamin and diagnostic parameters of PCOS were determined at early follicular phase. Afamin concentrations were significantly higher in patients with PCOS than in controls (odds ratio (OR) for a 10 mg/ml increase in afamin=1.3, 95% CI=1.08–1.58). This difference vanished in a model adjusting for age, BMI, free testosterone index (FTI), and sex hormone-binding globulin (SHBG) (OR=1.05, 95% CI=0.80–1.38). In patients with PCOS, afamin correlated significantly with homeostatic model assessment-insulin resistance (HOMA-IR), fasting glucose, BMI, FTI, and SHBG (P<0.001), but in a multivariate linear model, only HOMA-IR remained significantly associated with afamin (P=0.001). No correlation was observed between afamin and androgens, LH, FSH, LH/FSH ratio, antral follicle count, ovarian volume, or anti-Müllerian hormone. In conclusion, elevated afamin values may indicate a state of oxidative stress and inflammation, strongly associated with IR and offering an indicator of impaired glucose tolerance in patients with PCOS irrespective of obesity.
Search for other papers by Xingyan Liu in
Google Scholar
PubMed
Search for other papers by Mei Xu in
Google Scholar
PubMed
Search for other papers by Min Qian in
Google Scholar
PubMed
Search for other papers by Lindong Yang in
Google Scholar
PubMed
The cytochrome P450 family 17 (CYP17) is associated with hyperandrogenism in women, and the association between CYP17 gene polymorphism and the risk of polycystic ovary syndrome (PCOS) is not definitive. In order to determine whether the CYP17 T/C (rs74357) gene polymorphism is an exposure risk for PCOS, a comprehensive meta-analysis summarizing 19 studies was performed. The pooled odds ratio (OR) and the corresponding 95% CI were measured under five genetic models, and the stratified analyses by ethnicity, Hardy–Weinberg equilibrium, testosterone levels and BMI in controls were carried out to identify the causes of substantial heterogeneity. The overall results validated that the CYP17 T/C (rs74357) gene polymorphism was significantly associated with PCOS risk in four genetic models. Moreover, the outcomes of subgroup analysis by ethnicity indicated that the frequencies of the C allele of CYP17 T/C (rs74357) polymorphism were markedly higher in women from Asia than in Caucasians (T vs C: OR 0.85, 95% CI = 0.74–0.99, P < 0.05). Therefore, these findings suggested that the CYP17 T/C (rs74357) gene polymorphism played an indispensable part in increasing the susceptibility of PCOS when carrying the C allele, which proposed that the polymorphism of the CYP17 gene may be a predictive factor for the risk of PCOS or an important pathway in PCOS-associated metabolic and hormonal dysregulation.
Search for other papers by Silan Zheng in
Google Scholar
PubMed
Search for other papers by Meifeng Tong in
Google Scholar
PubMed
Search for other papers by Lianqin Dong in
Google Scholar
PubMed
Search for other papers by Chunmin Du in
Google Scholar
PubMed
Search for other papers by Xin Zheng in
Google Scholar
PubMed
Search for other papers by Liying Wang in
Google Scholar
PubMed
Search for other papers by Peiying Huang in
Google Scholar
PubMed
Search for other papers by Wei Liu in
Google Scholar
PubMed
Search for other papers by Mingzhu Lin in
Google Scholar
PubMed
The School of Clinical Medicine, Fujian Medical University, Fuzhou, China
Search for other papers by Changqin Liu in
Google Scholar
PubMed
Objective
To explore the independent associations of the new adiposity indices lipid accumulation product (LAP) index, visceral adiposity index (VAI), and product of triglycerides and glucose (TyG) with the risks of hepatic steatosis (HS) in women with polycystic ovary syndrome (PCOS).
Design
This is a cross-sectional study with 101 women with PCOS undergoing controlled attenuation parameter (CAP) measurement who were recruited from November 2018 to August 2019. Multivariable logistic regression analysis was performed to determine the associations of adiposity indices with HS.
Result(s)
Among the 101 PCOS patients, the prevalence rate of HS was 70.3%. The PCOS patients with HS have higher percentage of overweight/obesity status, higher level of aminotransferase (AST and ALT), homeostasis model assessment of insulin resistance (HOMA-IR), LAP, VAI, TyG, waist circumference (WC), and BMI (P < 0.05). Partial correlation analysis showed LAP, WC and BMI were significantly positively associated with CAP (P < 0.05) after controlling for confounding factors. Besides, BMI, WC, and CAP were gradually elevated with the increase of LAP level. Further, multivariable logistic regression analysis showed adjusted odd ratio (OR) with associated 95% CI (OR (95% CI)) were respectively 1.09 (1.03–1.16) for LAP, 1.14 (1.05–1.23) for WC, 1.28 (1.08–1.51) for BMI, respectively.
Conclusions
The present study demonstrates that in women with PCOS, except for the traditional adiposity indices (WC and BMI), LAP is independently correlated with the risk of HS.
Department of Gynecology and Reproductive Medicine, Karolinska University Hospital, Stockholm, Sweden.
Search for other papers by Angelica Lindén Hirschberg in
Google Scholar
PubMed
Emerging evidence indicates that testosterone, which can increase muscle mass and strength, stimulates erythropoiesis, promotes competitive behaviour, and enhances the physical performance of women. Indeed, the levels of testosterone within the normal female range are related to muscle mass and athletic performance in female athletes. Furthermore, among these athletes, the prevalence of hyperandrogenic conditions, including both polycystic ovary syndrome and rare differences/disorders of sex development (DSD), which may greatly increase testosterone production, are elevated. Thus, if the androgen receptors of an individual with XY DSD are functional, her muscle mass will develop like that of a man. These findings have led to the proposal that essential hyperandrogenism is beneficial for athletic performance and plays a role in the choice by women to compete in athletic activities. Moreover, a recent randomized controlled trial demonstrated a significant increase in the lean mass and aerobic performance by young exercising women when their testosterone levels were enhanced moderately. Circulating testosterone is considered the strongest factor to explain the male advantage in sport performance, ranging between 10 and 20%. It appears to be unfair to allow female athletes with endogenous testosterone levels in the male range (i.e. 10–20 times higher than normal) to compete against those with normal female androgen levels. In 2012, this consideration led international organizations to establish eligibility regulations for the female classification in order to ensure fair and meaningful competition, but the regulations are controversial and have been challenged in court.
Monash Centre for Health Research and Implementation, Monash University, Clayton, Victoria, Australia
Australian Institute for Musculoskeletal Science, Victoria University, Melbourne, Victoria, Australia
Medicine-Western Health, Faculty of Medicine, Dentistry and Health Science, Melbourne University, Melbourne, Victoria, Australia
Search for other papers by N K Stepto in
Google Scholar
PubMed
Search for other papers by D Hiam in
Google Scholar
PubMed
Search for other papers by M Gibson-Helm in
Google Scholar
PubMed
Search for other papers by S Cassar in
Google Scholar
PubMed
Search for other papers by C L Harrison in
Google Scholar
PubMed
Search for other papers by S K Hutchison in
Google Scholar
PubMed
Search for other papers by A E Joham in
Google Scholar
PubMed
Search for other papers by B J Canny in
Google Scholar
PubMed
Australian Institute for Musculoskeletal Science, Victoria University, Melbourne, Victoria, Australia
Search for other papers by A Moreno-Asso in
Google Scholar
PubMed
Division of Diabetes, Endocrinology & Gastroenterology, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK
Search for other papers by B J Strauss in
Google Scholar
PubMed
Search for other papers by N Hatzirodos in
Google Scholar
PubMed
Search for other papers by R J Rodgers in
Google Scholar
PubMed
Diabetes and Endocrine Units, Monash Health, Clayton, Victoria, Australia
Search for other papers by H J Teede in
Google Scholar
PubMed
Objective
Mechanisms of insulin resistance in polycystic ovary syndrome (PCOS) remain ill defined, contributing to sub-optimal therapies. Recognising skeletal muscle plays a key role in glucose homeostasis we investigated early insulin signalling, its association with aberrant transforming growth factor β (TGFβ)-regulated tissue fibrosis. We also explored the impact of aerobic exercise on these molecular pathways.
Methods
A secondary analysis from a cross-sectional study was undertaken in women with (n = 30) or without (n = 29) PCOS across lean and overweight BMIs. A subset of participants with (n = 8) or without (n = 8) PCOS who were overweight completed 12 weeks of aerobic exercise training. Muscle was sampled before and 30 min into a euglycaemic-hyperinsulinaemic clamp pre and post training.
Results
We found reduced signalling in PCOS of mechanistic target of rapamycin (mTOR). Exercise training augmented but did not completely rescue this signalling defect in women with PCOS. Genes in the TGFβ signalling network were upregulated in skeletal muscle in the overweight women with PCOS but were unresponsive to exercise training except for genes encoding LOX, collagen 1 and 3.
Conclusions
We provide new insights into defects in early insulin signalling, tissue fibrosis, and hyperandrogenism in PCOS-specific insulin resistance in lean and overweight women. PCOS-specific insulin signalling defects were isolated to mTOR, while gene expression implicated TGFβ ligand regulating a fibrosis in the PCOS-obesity synergy in insulin resistance and altered responses to exercise. Interestingly, there was little evidence for hyperandrogenism as a mechanism for insulin resistance.
Search for other papers by Carla Scaroni in
Google Scholar
PubMed
Search for other papers by Nora M Albiger in
Google Scholar
PubMed
Search for other papers by Serena Palmieri in
Google Scholar
PubMed
Search for other papers by Davide Iacuaniello in
Google Scholar
PubMed
Search for other papers by Chiara Graziadio in
Google Scholar
PubMed
Search for other papers by Luca Damiani in
Google Scholar
PubMed
Search for other papers by Marialuisa Zilio in
Google Scholar
PubMed
Search for other papers by Antonio Stigliano in
Google Scholar
PubMed
Search for other papers by Annamaria Colao in
Google Scholar
PubMed
Search for other papers by Rosario Pivonello in
Google Scholar
PubMed
Search for other papers by the Altogether to Beat Cushing’s Syndrome (ABC) study group in
Google Scholar
PubMed
The distinction between pseudo-Cushing’s states (PCS) and Cushing’s syndrome (CS) poses a significant clinical challenge even for expert endocrinologists. A patient’s clinical history can sometimes help to distinguish between them (as in the case of alcoholic individuals), but the overlap in clinical and laboratory findings makes it difficult to arrive at a definitive diagnosis. We aim to describe the most common situations that can give rise to a condition resembling overt endogenous hypercortisolism and try to answer questions that physicians often face in clinical practice. It is important to know the relative prevalence of these different situations, bearing in mind that most of the conditions generating PCS are relatively common (such as metabolic syndrome and polycystic ovary syndrome), while CS is rare in the general population. Physicians should consider CS in the presence of additional features. Appropriate treatment of underlying conditions is essential as it can reverse the hormonal abnormalities associated with PCS. Close surveillance and a thorough assessment of a patient’s hormone status will ultimately orient the diagnosis and treatment options over time.
Search for other papers by Ewa Stogowska in
Google Scholar
PubMed
Search for other papers by Karol Adam Kamiński in
Google Scholar
PubMed
Search for other papers by Bartosz Ziółko in
Google Scholar
PubMed
Search for other papers by Irina Kowalska in
Google Scholar
PubMed
The subject of vocal changes accompanying pathological conditions, although still not well explored, seems to be promising. The discovery of laryngeal receptors for sex hormones and thyroid hormones can strongly support the hypothesis of changes in voice due to various endocrinopathies. On the other hand, the impairment of the proper function of the vocal apparatus can also be caused in the process of the microvasculature complications of diabetes mellitus. This review was a comprehensive summary of the accessible literature concerning the influence of selected endocrinopathies on subjective and objective voice parameters. We analysed a total number of 16 English-language research papers from the PubMed database, released between 2008 and 2021, describing vocal changes in reproductive disorders such as polycystic ovary syndrome and congenital adrenal hyperplasia, thyroid disorders in shape of hypo- or hyperthyroidism and type 2 diabetes mellitus. The vast majority of the analysed articles proved some changes in voice in all mentioned conditions, although the detailed affected vocal parameters frequently differed between research. We assume that the main cause of the observed conflicting results might stem from non-homogeneous methodology designs of the analysed studies.
Search for other papers by Hong Tang in
Google Scholar
PubMed
Search for other papers by Xiaomei Jiang in
Google Scholar
PubMed
Search for other papers by Yu Hua in
Google Scholar
PubMed
Search for other papers by Heyue Li in
Google Scholar
PubMed
Search for other papers by Chunlan Zhu in
Google Scholar
PubMed
Search for other papers by Xiaobai Hao in
Google Scholar
PubMed
Search for other papers by Minhui Yi in
Google Scholar
PubMed
Search for other papers by Linxia Li in
Google Scholar
PubMed
Background
Polycystic ovary syndrome (PCOS) is an androgen disorder and ovarian dysfunction disease in women of reproductive age. The cell death of granulosa cells (GCs) plays an important role in the development of PCOS. However, the mechanism of GC death is still unclear.
Methods
In the current study, NEDD4L was found to be elevated in PCOS GEO (Gene Expression Omnibus) databases and mouse models. The cell viability was analyzed by CCK-8 and FDA staining. The expression of ferroptosis markers was assessed by ELISA and immunofluorescence. The direct interaction of GPX4 and NEDD4L was verified by co-immunoprecipitation assay.
Result
Functionally, results from CCK-8 and FDA staining demonstrated that NEDD4L inhibited the cell viability of KGN cells and NEDD4L increased the levels of iron, malonyldialdehyde, and reactive oxygen species and decreased glutathione levels. Moreover, the cell death of KGN induced by NEDD4L was blocked by ferroptosis inhibitor, suggesting that NEDD4L regulates KGN cell ferroptosis. Mechanistically, NEDD4L directly interacts with GPX4 and promotes GPX4 ubiquitination and degradation.
Conclusion
Taken together, our study indicated that NEDD4L facilitates GC ferroptosis by promoting GPX4 ubiquitination and degradation and contributes to the development of PCOS.
Fujian Maternal-Fetal Clinical Medicine Research Center, Fuzhou, China
Fujian Key Laboratory of Prenatal Diagnosis and Birth Defect, Fuzhou, China
Search for other papers by Xiuhua Liao in
Google Scholar
PubMed
Search for other papers by Suqin Zhu in
Google Scholar
PubMed
Search for other papers by Shumin Qiu in
Google Scholar
PubMed
Search for other papers by Hua Cao in
Google Scholar
PubMed
Search for other papers by Wenwen Jiang in
Google Scholar
PubMed
Search for other papers by Huiling Xu in
Google Scholar
PubMed
Search for other papers by Yan Sun in
Google Scholar
PubMed
Fujian Maternal-Fetal Clinical Medicine Research Center, Fuzhou, China
Fujian Key Laboratory of Prenatal Diagnosis and Birth Defect, Fuzhou, China
Search for other papers by Beihong Zheng in
Google Scholar
PubMed
This study aimed to investigate the role of mitochondrial-related protein Mfn2 in polycystic ovary syndrome (PCOS) and its impact on oocyte development. The pathological features of PCOS model mice were confirmed by hematoxylin–eosin staining and immunohistochemistry. The expression of Mfn2 and mitochondrial-related proteins in PCOS oocytes and granulosa cells was detected by qRT-PCR and Western blot. Mitochondrial quantity was measured by Mito-Tracker staining, and the structure of mitochondria-associated ER membranes (MAMs) was observed by transmission electron microscopy. The results showed that Mfn2 was significantly downregulated in PCOS oocytes and granulosa cells, and its expression was inhibited in oocytes at different developmental stages. Moreover, the structure of MAMs was also disrupted. Downregulation of Mfn2 expression led to a reduction in mitochondrial quantity in oocytes and granulosa cells, as well as disruption of MAM structure, while overexpression of Mfn2 had the opposite effect. In conclusion, this study indicates that Mfn2 affects the development of PCOS oocytes by regulating MAMs and may be involved in maintaining the stability of MAM structure and function, thereby affecting mitochondrial quantity and function. These findings provide new insights into the pathogenesis and treatment of PCOS.
Search for other papers by Charissa van Zwol-Janssens in
Google Scholar
PubMed
Search for other papers by Aglaia Hage in
Google Scholar
PubMed
Search for other papers by Kim van der Ham in
Google Scholar
PubMed
Search for other papers by Birgitta K Velthuis in
Google Scholar
PubMed
Search for other papers by Ricardo P J Budde in
Google Scholar
PubMed
Search for other papers by Maria P H Koster in
Google Scholar
PubMed
Search for other papers by Arie Franx in
Google Scholar
PubMed
Search for other papers by Bart C J M Fauser in
Google Scholar
PubMed
Search for other papers by Eric Boersma in
Google Scholar
PubMed
Department of Epidemiology, Erasmus University Medical Center, Rotterdam, the Netherlands
Search for other papers by Daniel Bos in
Google Scholar
PubMed
Search for other papers by Joop S E Laven in
Google Scholar
PubMed
Search for other papers by Yvonne V Louwers in
Google Scholar
PubMed
Search for other papers by the CREW consortium in
Google Scholar
PubMed
Besides age, estrogen exposure plays a crucial role in changes in bone density (BD) in women. Premature ovarian insufficiency (POI) and polycystic ovary syndrome (PCOS) are conditions in reproductive-aged women in which the exposure to estrogen is substantially different. Women with a history of preeclampsia (PE) are expected to have normal estrogen exposure. Within the CREw-IMAGO study, we investigated if trabecular BD is different in these women because of differences in the duration of estrogen exposure. Trabecular BD was measured in thoracic vertebrae on coronary CT scans. Women with a reduced estrogen exposure (POI) have a lower BD compared to women with an intermediate exposure (PE) (mean difference (MD) −26.8, 95% CI −37.2 to −16.3). Women with a prolonged estrogen exposure (PCOS) have the highest BD (MD 15.0, 95% CI 4.3–25.7). These results support the hypothesis that the duration of estrogen exposure in these women is associated with trabecular BD.
Significance statement
Our results suggest that middle-aged women with PCOS have a higher BD and women with POI have a lower BD. We hypothesized that this is due to either a prolonged estrogen exposure, as seen in women with PCOS, or a reduced estrogen exposure, as in women with POI. In the counseling of women with reproductive disorders on long-term health issues, coronary CT provides a unique opportunity to assess both coronary artery calcium score for cardiovascular screening as well as trabecular BD.
