Search Results
You are looking at 71 - 80 of 238 items for
- Abstract: adrenarche x
- Abstract: amenorrhoea x
- Abstract: fertility x
- Abstract: Gender x
- Abstract: Hypogonadism x
- Abstract: infertility x
- Abstract: Klinefelter x
- Abstract: menarche x
- Abstract: menopause x
- Abstract: transsexual x
- Abstract: Turner x
- Abstract: sperm* x
- Abstract: ovary x
- Abstract: follicles x
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.
Search for other papers by Junhui Zhang in
Google Scholar
PubMed
Search for other papers by Hongyan Zhang in
Google Scholar
PubMed
Search for other papers by Bao Guo in
Google Scholar
PubMed
Search for other papers by Jun Yang in
Google Scholar
PubMed
Search for other papers by Renxiang Yu in
Google Scholar
PubMed
Search for other papers by Wenxiu Chen in
Google Scholar
PubMed
Search for other papers by Muxin Zhai in
Google Scholar
PubMed
Search for other papers by Cao Yuhan in
Google Scholar
PubMed
Search for other papers by Yajing Liu in
Google Scholar
PubMed
Search for other papers by Qiang Hong in
Google Scholar
PubMed
Search for other papers by Fenfen Xie in
Google Scholar
PubMed
The elevated level of hepatic oxidative stress (OS) in polycystic ovary syndrome (PCOS) is one of the important causes of liver abnormalities. Therefore, decreasing the level of hepatic OS in PCOS is beneficial to reduce the risk of PCOS-related liver diseases. Melatonin (MT), recognized as a potent antioxidant. Nevertheless, the efficacy of MT in alleviating hepatic OS associated with PCOS is yet to be established, and the precise mechanisms through which MT exerts its antioxidant effects remain to be fully elucidated. The aim of this study was to explore the potential mechanism by which MT reduces hepatic OS in PCOS. First, we detected elevated OS levels in the PCOS samples. Subsequently, with MT pretreatment, we discovered that MT could significantly diminish the levels of OS, liver triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT) and aspartate aminotransferase (AST)，while concurrently ameliorating mitochondrial structural damage in PCOS liver. Furthermore, we identified elevated autophagy levels in the liver of PCOS rats and an inhibition of the Keap1-Nrf2 pathway. Through MT pretreatment, the expression of LC3 was significantly decreased, while the Keap1-Nrf2 pathway was activated. Our study showed that MT could affect the Nrf2 pathway dependent on the P62/LC3 autophagy pathway, thereby attenuating hepatic OS in PCOS. These findings offer novel insights and research avenues for the study of PCOS-related liver diseases.
Disciplina de Endocrinologia, Faculdade de Ciências Médicas da Santa Casa de São Paulo, São Paulo, São Paulo, Brazil
Unidade de Endocrinologia do Desenvolvimento, Laboratorio de Hormonios e Genetica Molecular LIM/42, Disciplina de Endocrinologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, São Paulo, Brazil
Search for other papers by Renata C Scalco in
Google Scholar
PubMed
Search for other papers by Ericka B Trarbach in
Google Scholar
PubMed
Search for other papers by Edoarda V A Albuquerque in
Google Scholar
PubMed
Search for other papers by Thais K Homma in
Google Scholar
PubMed
Search for other papers by Thais H Inoue-Lima in
Google Scholar
PubMed
Search for other papers by Mirian Y Nishi in
Google Scholar
PubMed
Search for other papers by Berenice B Mendonca in
Google Scholar
PubMed
Search for other papers by Alexander A L Jorge in
Google Scholar
PubMed
Most patients with Turner syndrome (TS) need hormone replacement therapy because of hypergonadotropic hypogonadism; individual outcomes, however, are highly variable. Our objective was to assess the influence of five estrogen receptor 1 gene (ESR1) polymorphisms (rs543650, rs1038304, rs2046210, rs2234693 and rs9340799) on adult height, breast development, uterine volume and bone mineral density (BMD). We studied 91 TS patients from a tertiary hospital using adult estrogen dose. In our group, ESR1 rs2234693 was associated with femoral neck and total hip BMD, and it accounted for around 10% of BMD variability in both sites (P < 0.01). Patients homozygous for C allele in this polymorphism had significantly lower femoral neck BMD (0.699 ± 0.065 g/cm2 vs 0.822 ± 0.113 g/cm2, P = 0.008) and total hip BMD (0.777 ± 0.118 g/cm2 vs 0.903 ± 0.098 g/cm2, P = 0.009) than patients homozygous for T allele. The other four ESR1 polymorphisms were not able to predict any of the above estrogen therapy outcomes in an isolated manner. Patients homozygous for the haplotype GCG formed by polymorphisms rs543650, rs2234693 and rs9340799 had an even more significantly lower femoral neck BMD (0.666 ± 0.049 vs 0.820 ± 0.105 g/cm2, P = 0.0047) and total hip BMD (0.752 ± 0.093 vs 0.908 ± 0.097 g/cm2, P = 0.0029) than patients homozygous for haplotypes with a T allele in rs2234693. In conclusion, homozygosity for C allele in ESR1 rs2234693 and/or for GCG haplotype appears to be associated with lower femoral neck and total hip BMD. We believe that the identification of polymorphisms related to estrogen outcomes may contribute to individualization of treatment in TS.
Search for other papers by Jan Roar Mellembakken in
Google Scholar
PubMed
Search for other papers by Azita Mahmoudan in
Google Scholar
PubMed
Search for other papers by Lars Mørkrid in
Google Scholar
PubMed
Search for other papers by Inger Sundström-Poromaa in
Google Scholar
PubMed
Search for other papers by Laure Morin-Papunen in
Google Scholar
PubMed
Department of Obstetrics and Gynecology, Helsinki University Hospital and University of Helsinki, Helsinki, Uusimaa, Finland
Search for other papers by Juha S Tapanainen in
Google Scholar
PubMed
Search for other papers by Terhi T Piltonen in
Google Scholar
PubMed
Search for other papers by Angelica Lindén Hirschberg in
Google Scholar
PubMed
Search for other papers by Elisabet Stener-Victorin in
Google Scholar
PubMed
Department of Gynecology and Obstetrics, St. Olav’s Hospital, Trondheim, Norway
Search for other papers by Eszter Vanky in
Google Scholar
PubMed
Search for other papers by Pernille Ravn in
Google Scholar
PubMed
Search for other papers by Richard Christian Jensen in
Google Scholar
PubMed
Search for other papers by Marianne Skovsager Andersen in
Google Scholar
PubMed
Search for other papers by Dorte Glintborg in
Google Scholar
PubMed
Objective
Obesity is considered to be the strongest predictive factor for cardio-metabolic risk in women with polycystic ovary syndrome (PCOS). The aim of the study was to compare blood pressure (BP) in normal weight women with PCOS and controls matched for age and BMI.
Methods
From a Nordic cross-sectional base of 2615 individuals of Nordic ethnicity, we studied a sub cohort of 793 normal weight women with BMI < 25 kg/m2 (512 women with PCOS according to Rotterdam criteria and 281 age and BMI-matched controls). Participants underwent measurement of BP and body composition (BMI, waist-hip ratio), lipid status, and fasting BG. Data were presented as median (quartiles).
Results
The median age for women with PCOS were 28 (25, 32) years and median BMI was 22.2 (20.7, 23.4) kg/m2. Systolic BP was 118 (109, 128) mmHg in women with PCOS compared to 110 (105, 120) mmHg in controls and diastolic BP was 74 (67, 81) vs 70 (64, 75) mmHg, both P < 0.001. The prevalence of women with BP ≥ 140/90 mmHg was 11.1% (57/512) in women with PCOS vs 1.8% (5/281) in controls, P < 0.001. In women ≥ 35 years the prevalence of BP ≥ 140/90 mmHg was comparable in women with PCOS and controls (12.7% vs 9.8%, P = 0.6). Using multiple regression analyses, the strongest association with BP was found for age, waist circumference, and total cholesterol in women with PCOS.
Conclusions
Normal weight women with PCOS have higher BP than controls. BP and metabolic screening are relevant also in young normal weight women with PCOS.
Search for other papers by Feifei Cheng in
Google Scholar
PubMed
Search for other papers by Noel Yat Hey Ng in
Google Scholar
PubMed
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Search for other papers by Claudia Ha Ting Tam in
Google Scholar
PubMed
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Search for other papers by Yuying Zhang in
Google Scholar
PubMed
Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Search for other papers by Cadmon King Poo Lim in
Google Scholar
PubMed
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Search for other papers by Guozhi Jiang in
Google Scholar
PubMed
Search for other papers by Alex Chi Wai Ng in
Google Scholar
PubMed
Search for other papers by Tiffany Tse Ling Yau in
Google Scholar
PubMed
Search for other papers by Lai Ping Cheung in
Google Scholar
PubMed
State Key Laboratory of Pharmaceutical Biotechnology, University of Hong Kong, Hong Kong, Hong Kong
Department of Pharmacy and Pharmacology, LKS Faculty of Medicine, University of Hong Kong, Hong Kong, Hong Kong
Search for other papers by Aimin Xu in
Google Scholar
PubMed
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Chinese University of Hong Kong-Shanghai Jiao Tong University Joint Research Centre in Diabetes Genomics and Precision Medicine, Hong Kong, Hong Kong
Search for other papers by Juliana C N Chan in
Google Scholar
PubMed
Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
Chinese University of Hong Kong-Shanghai Jiao Tong University Joint Research Centre in Diabetes Genomics and Precision Medicine, Hong Kong, Hong Kong
Search for other papers by Ronald C W Ma in
Google Scholar
PubMed
Women with polycystic ovary syndrome (PCOS) have an increased risk of developing type 2 diabetes. FGF19, FGF21 and lipocalin-2 have emerged as important markers of metabolic risk. This study aims to compare the levels of FGF19, FGF21 and lipocalin-2 between subjects with or without PCOS, and to investigate the relationship between proteins and diabetes progression. In this nested case–control cohort study, 128 Chinese PCOS women and 128 controls were recruited and followed-up. All subjects underwent the oral glucose tolerance test for the evaluation of glycaemic status. Baseline serum protein levels were measured using ELISA. Compared with controls, PCOS subjects had higher levels of FGF19 (P < 0.001) and FGF21 (P = 0.022), but had lower lipocalin-2 (P < 0.001). In total, 20.8% of PCOS and 9.2% of controls developed diabetes over a mean duration of 10.4 ± 1.2 and 11.3 ± 0.5 years, respectively. Logistic regression analyses suggested FGF19 was positively associated with diabetes progression in controls, after adjusting for age, follow-up duration, waist and fasting glucose (P = 0.026, odds ratio (OR) (95% CI): 7.4 (1.3–43.6)), and the positive relationship between FGF21 and diabetes progression in controls was attenuated by adjusting for age and follow-up duration (P = 0.183). Lipocalin-2 was positively correlated with diabetes progression in PCOS group (P = 0.026, OR (95% CI)): 2.5 (1.1–5.6)); however, this became attenuated after adjusting for waist and fasting glucose (P = 0.081). In conclusion, there is differential expression of FGF19, FGF21, and lipocalin-2 in PCOS. The serum level of FGF19, and FGF21 is associated with diabetes progression in women without PCOS, while lipocalin-2 was related to diabetes progression in PCOS women.
Search for other papers by Mírian Romitti in
Google Scholar
PubMed
Search for other papers by Vitor C Fabris in
Google Scholar
PubMed
Search for other papers by Patricia K Ziegelmann in
Google Scholar
PubMed
Search for other papers by Ana Luiza Maia in
Google Scholar
PubMed
Search for other papers by Poli Mara Spritzer in
Google Scholar
PubMed
Polycystic ovary syndrome (PCOS) is the most prevalent endocrine disorder affecting women of reproductive age. PCOS has been associated with distinct metabolic and cardiovascular diseases and with autoimmune conditions, predominantly autoimmune thyroid disease (AITD). AITD has been reported in 18–40% of PCOS women, depending on PCOS diagnostic criteria and ethnicity. The aim of this systematic review and meta-analysis was to summarize the available evidence regarding the likelihood of women with PCOS also having AITD in comparison to a reference group of non-PCOS women. We systematically searched EMBASE and MEDLINE for non-interventional case control, cross-sectional or cohort studies published until August 2017. The Ottawa–Newcastle Scale was used to assess the methodological quality of studies. Statistical meta-analysis was performed with R. Thirteen studies were selected for the present analysis, including 1210 women diagnosed with PCOS and 987 healthy controls. AITD was observed in 26.03 and 9.72% of PCOS and control groups respectively. A significant association was detected between PCOS and chance of AITD (OR = 3.27, 95% CI 2.32–4.63). Notably, after geographical stratification, the higher risk of AITD in PCOS women persisted for Asians (OR = 4.56, 95% CI 2.47–8.43), Europeans (OR = 3.27, 95% CI 2.07–5.15) and South Americans (OR = 1.86, 95% CI 1.05–3.29). AIDT is a frequent condition in PCOS patients and might affect thyroid function. Thus, screening for thyroid function and thyroid-specific autoantibodies should be considered in patients with PCOS even in the absence of overt symptoms. This systematic review and meta-analysis is registered in PROSPERO under number CRD42017079676.
Search for other papers by Angela Köninger in
Google Scholar
PubMed
Search for other papers by Antonella Iannaccone in
Google Scholar
PubMed
Search for other papers by Ensar Hajder in
Google Scholar
PubMed
Search for other papers by Mirjam Frank in
Google Scholar
PubMed
Search for other papers by Boerge Schmidt in
Google Scholar
PubMed
Search for other papers by Ekkehard Schleussner in
Google Scholar
PubMed
Search for other papers by Rainer Kimmig in
Google Scholar
PubMed
Search for other papers by Alexandra Gellhaus in
Google Scholar
PubMed
Search for other papers by Hans Dieplinger in
Google Scholar
PubMed
Background
Patients suffering from polycystic ovary syndrome (PCOS) are often insulin resistant and at elevated risk for developing gestational diabetes mellitus (GDM). The aim of this study was to explore afamin, which can be determined preconceptionally to indicate patients who will subsequently develop GDM. Serum concentrations of afamin are altered in conditions of oxidative stress like insulin resistance (IR) and correlate with the gold standard of IR determination, the HOMA index.
Methods
Afamin serum concentrations and the HOMA index were analyzed post hoc in 63 PCOS patients with live births. Patients were treated at Essen University Hospital, Germany, between 2009 and 2018. Mann–Whitney U test, T test, Spearman’s correlation, linear regression models and receiver-operating characteristic (ROC) analyses were performed for statistical analysis.
Results
Patients who developed GDM showed significantly higher HOMA and serum afamin values before their pregnancy (P < 0.001, respectively). ROCs for afamin concentrations showed an area under the curve of 0.78 (95% confidence interval (CI) 0.65–0.90) and of 0.77 (95% CI 0.64–0.89) for the HOMA index. An afamin threshold of 88.6 mg/L distinguished between women who will develop GDM and those who will not with a sensitivity of 79.3% and a specificity of 79.4%. A HOMA index of 2.5 showed a sensitivity of 65.5% and a specificity of 88.2%.
Conclusion
The HOMA index and its surrogate parameter afamin are able to identify pre-pregnant PCOS patients who are at risk to develop GDM. Serum afamin concentrations are independent of fasting status and therefore an easily determinable biomarker.
Polish Mother’s Memorial Hospital–Research Institute, Lodz, Poland
Search for other papers by Krzysztof C Lewandowski in
Google Scholar
PubMed
Search for other papers by Justyna Płusajska in
Google Scholar
PubMed
Search for other papers by Wojciech Horzelski in
Google Scholar
PubMed
Search for other papers by Ewa Bieniek in
Google Scholar
PubMed
Polish Mother’s Memorial Hospital–Research Institute, Lodz, Poland
Search for other papers by Andrzej Lewiński in
Google Scholar
PubMed
Background
Though insulin resistance (IR) is common in polycystic ovary syndrome (PCOS), there is no agreement as to what surrogate method of assessment of IR is most reliable.
Subjects and methods
In 478 women with PCOS, we compared methods based on fasting insulin and either fasting glucose (HOMA-IR and QUICKI) or triglycerides (McAuley Index) with IR indices derived from glucose and insulin during OGTT (Belfiore, Matsuda and Stumvoll indices).
Results
There was a strong correlation between IR indices derived from fasting values HOMA-IR/QUICKI, r = −0.999, HOMA-IR/McAuley index, r = −0.849 and between all OGTT-derived IR indices (e.g. r = −0.876, for IRI/Matsuda, r = −0.808, for IRI/Stumvoll, and r = 0.947, for Matsuda/Stumvoll index, P < 0.001 for all), contrasting with a significant (P < 0.001), but highly variable correlation between IR indices derived from fasting vs OGTT-derived variables, ranging from r = −0.881 (HOMA-IR/Matsuda), through r = 0.58, or r = −0.58 (IRI/HOMA-IR, IRI/QUICKI, respectively) to r = 0.41 (QUICKI/Stumvoll), and r = 0.386 for QUICKI/Matsuda indices. Detailed comparison between HOMA-IR and IRI revealed that concordance between HOMA and IRI was poor for HOMA-IR/IRI values above 75th and 90th percentile. For instance, only 53% (70/132) women with HOMA-IR >75th percentile had IRI value also above 75th percentile. There was a significant, but weak correlation of all IR indices with testosterone concentrations.
Conclusions
Significant number of women with PCOS can be classified as being either insulin sensitive or insulin resistant depending on the method applied, as correlation between various IR indices is highly variable. Clinical application of surrogate indices for assessment of IR in PCOS must be therefore viewed with an extreme caution.
Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Malin Nylander in
Google Scholar
PubMed
Department of Internal Medicine, Endocrine Unit, Herlev Gentofte Hospital, Herlev, Denmark
Search for other papers by Signe Frøssing in
Google Scholar
PubMed
Department of Internal Medicine, Endocrine Unit, Herlev Gentofte Hospital, Herlev, Denmark
Search for other papers by Caroline Kistorp in
Google Scholar
PubMed
Department of Internal Medicine, Endocrine Unit, Herlev Gentofte Hospital, Herlev, Denmark
Search for other papers by Jens Faber in
Google Scholar
PubMed
Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Sven O Skouby in
Google Scholar
PubMed
Polycystic ovary syndrome (PCOS) is associated with increased risk of venous thromboembolism (VTE) and cardiovascular disease (CVD) in later life. We aimed to study the effect of liraglutide intervention on markers of VTE and CVD risk, in PCOS. In a double-blind, placebo-controlled, randomized trial, 72 overweight and/or insulin-resistant women with PCOS were randomized, in a 2:1 ratio, to liraglutide or placebo 1.8 mg/day. Endpoints included between-group difference in change (baseline to follow-up) in plasminogen activator inhibitor-1 levels and in thrombin generation test parameters: endogenous thrombin potential, peak thrombin concentration, lag time and time to peak. Mean weight loss was 5.2 kg (95% CI 3.0–7.5 kg, P < 0.001) in the liraglutide group compared with placebo. We detected no effect on endogenous thrombin potential in either group. In the liraglutide group, peak thrombin concentration decreased by 16.71 nmol/L (95% CI 2.32–31.11, P < 0.05) and lag time and time to peak increased by 0.13 min (95% CI 0.01–0.25, P < 0.05) and 0.38 min (95% CI 0.09–0.68, P < 0.05), respectively, but there were no between-group differences. There was a trend toward 12% (95% CI 0–23, P = 0.05) decreased plasminogen activator inhibitor-1 in the liraglutide group, and there was a trend toward 16% (95% CI −4 to 32, P = 0.10) reduction, compared with placebo. In overweight women with PCOS, liraglutide intervention caused an approximate 5% weight loss. In addition, liraglutide affected thrombin generation, although not significantly differently from placebo. A concomitant trend toward improved fibrinolysis indicates a possible reduction of the baseline thrombogenic potential. The findings point toward beneficial effects of liraglutide on markers of VTE and CVD risk, which should be further pursued in larger studies.
