Mechanism Of Polycystic Ovary Syndrome Research Articles

Exogenous testosterone does not induce or exacerbate the metabolic features associated with PCOS among transgender men

Objective: Polycystic ovary syndrome (PCOS) is a complex condition which can include menstrual irregularity, metabolic derangement, and increased androgen levels. The mechanism of PCOS is unknown. Some suggest that excess production of androgens by the ovaries may cause or exacerbate the metabolic findings. The purpose of this study was to assess the role of increased testosterone on metabolic parameters for individuals presumed to be chromosomally female by examination of these parameters in hormone-treated transgender men. Methods: In 2015 and 2016, we asked all transgender men who visited the Endocrinology Clinic at Boston Medical Center treated with testosterone for consent for a retrospective anonymous chart review. Of the 36 men, 34 agreed (94%). Serum metabolic factors and body mass index (BMI) levels for each patient were graphed over time, from initiation of therapy through 6 years of treatment. Bivariate analyses were conducted to analyze the impact of added testosterone. Results: Regressions me...

Fluorine may intensify the mechanisms of polycystic ovary syndrome (PCOS) development via increased insulin resistance and disturbed thyroid-stimulating hormone (TSH) synthesis even at reference levels

We were interested whether fluorine, at the concentrations regarded as normal, can play a role in PCOS pathogenesis. The effect was not described in PCOS.Women with PCOS were diagnosed according to Rotterdam's criteria. The average age of 40 examined women with PCOS was 26.3 ± 5.5 years, BMI-29.16 ± 0.8, WHR-0.91 ± 0.08.Main Outcome Measures: ECLIA was used to analyse testosterone, FSH, LH, oestradiol, TSH, prolactin, insulin and SHBG. Fluorine content was analysed by potentiometry using ion selective electrode.Fluorine content in serum of women with PCOS did not statistically significantly differ from that of the control group and amounted to 0.224 ± 0.043 and 0.228 ± 0.023 ppm, respectively. There were significant differences in the levels of TSH and HOMA-IR between the groups.Based on the correlation matrix, a negative correlation with the level of SHBG protein and the level of glucose on fasting was showed for the group with a lower of fluorine, and a positive correlation with HDL level was observed in the group with higher concentration of fluorine. In the phenotype with a higher level of androgens, there was a negative correlation with triglycerides level and a positive correlation with HDL.Fluorine, even in concentrations regarded as proper, takes part in PCOS pathogenesis. It increases the synthesis of TSH and increases insulin resistance. Higher insulin resistance leads to the reduced synthesis of SHBG transport protein. Therefore, the key factor in PCOS pathogenesis is testosterone, but fluorine facilitates disruptions in carbohydrates and lipids metabolism leading to increased levels of androgens in blood.

EXOGENOUS TESTOSTERONE DOES NOT INDUCE OR EXACERBATE THE METABOLIC FEATURES ASSOCIATED WITH PCOS AMONG TRANSGENDER MEN

Polycystic ovary syndrome (PCOS) is a complex condition which can include menstrual irregularity, metabolic derangement, and increased androgen levels. The mechanism of PCOS is unknown. Some suggest that excess production of androgens by the ovaries may cause or exacerbate the metabolic findings. The purpose of this study was to assess the role of increased testosterone on metabolic parameters for individuals presumed to be chromosomally female by examination of these parameters in hormone-treated transgender men. In 2015 and 2016, we asked all transgender men who visited the Endocrinology Clinic at Boston Medical Center treated with testosterone for consent for a retrospective anonymous chart review. Of the 36 men, 34 agreed (94%). Serum metabolic factors and body mass index (BMI) levels for each patient were graphed over time, from initiation of therapy through 6 years of treatment. Bivariate analyses were conducted to analyze the impact of added testosterone. Regressions measuring the impact of testosterone demonstrated no significant changes in levels of glycated hemoglobin (HbA1c), triglycerides, or low-density-lipoprotein cholesterol. There was a statistically significant decrease in BMI with increasing testosterone. There was also a statistically significant decrease in high-density lipoprotein levels upon initiation of testosterone therapy. Testosterone therapy in transgender men across a wide range of doses and over many years did not result in the dyslipidemia or abnormalities in HbA1c seen with PCOS. Instead, treatment of transgender men with testosterone resulted only in a shift of metabolic biomarkers toward the average physiologic male body. BMI = body mass index; HbA1c = glycated hemoglobin; HDL = high-density lipoprotein; LDL = low-density lipoprotein; PCOS = polycystic ovary syndrome.

Establishment of a model of dihydrotestosterone-induced polycystic ovary syndrome complicated with atherosclerosis in rats

Objective To establish a rat model of polycystic ovary syndrome(PCOS) complicated with atherosclerosis(AS). Methods Sixteen female SD rats were selected and randomly divided into control group and model group, with 8 rats in each group.The rats in the control group were given routine rearing.The rats in the model group were subcutaneously given dihydrotestosterone(DHT) in neck and fed with high fat diet for a long term.The changes of food intake (FI), body weight(BW), testosterone (T), estrogen (E2), luteinizing hormone (LH), total cholesterol (TC), blood glucose (BG) and insulin (INS) were observed in the two groups. Results The levels of FI, T, E2, LH between the control group and model group had no obvious change[(86.13±7.83)g/r vs.(96.25±10.66)g/r, t=2.113, P=0.563, (10.79±1.74)mg/L vs.(11.47±1.89)mg/L, t=1.785, P=0.087; (36.58±2.57)ng/L vs.(38.64±1.78)ng/L, t=2.697, P=0.068; (15.47±1.96)IU/L vs.(16.01±0.80)IU/L, t=1.570, P=0.614]. The levels of BW, TC, DHT, INS in the model group were significantly higher than those in the control group[(234.54±17.14)g vs.(192.67±16.47)g, t=7.930, P<0.000; (2.47±0.13)mmol/L vs.(2.02±0.15)mmol/L, t=6.475, P<0.000; (139.75±12.12)ng/L vs.(55.63±7.80)ng/L, t=8.697, P<0.000; (283.25±33.47)pg/mg vs.(162.12±15.51)pg/mg, t=9.289, P<0.000]. Tube wall was markedly thickened in the model group after being given high fat feed for 12 weeks, and intimal wall was significantly thickened after 16 weeks, and endotheliocyte injury, deep collagen fiber, monocyte adhesion, visible atherosclerotic plaques were observed in the model grouop. Conclusion DHT-induced PCOS rat model by high fat feed reproduces the human typical clinical symptoms and pathological characteristics, it can provide a relatively simple and feasible rat model for further study of the mechanism of PCOS complicated with AS. Key words: Polycystic ovary syndrome; Dihydrotestosterone; Atherosclerosis; Rats; Models, animal

Failure of Gnrh Agonist to Trigger Ovulation: A Clue to the Mechanism of Polycystic Ovary Syndrome?

Failure of Gnrh Agonist to Trigger Ovulation: A Clue to the Mechanism of Polycystic Ovary Syndrome?

Novel Serum Biomarkers Detected by Protein Array in Polycystic Ovary Syndrome with Low Progesterone Level

Background/Aims: Polycystic ovary syndrome (PCOS), characterized by female infertility and metabolic abnormalities, is one of the most common endocrine disorders. The etiology of PCOS remains unknown. The comprehensive analysis of protein alterations in PCOS patients is meaningful for identifying diagnostic biomarkers of PCOS. Here, we explored the clinical value of serum proteins as novel biomarkers to detect PCOS with low progesterone level. Methods: A total of 43 patients with PCOS and 30 healthy women were enrolled. Protein array was used to detect the variations of serum proteins between PCOS patients and healthy women. The level of five serum proteins was further confirmed by ELISA and western blot. The human ovarian granulosa cells (KGN) was cultured to examine the underlying mechanism of PCOS. CCK8 assay and western blot were carried out to evaluate the alterations in proliferative ability, TUNEL assay and DAPI staining to detect the apoptosis of KGN cells. Results: Among the 507 proteins, we identified 76 differentially expressed serum proteins (≧1.5 fold), with 40 elevated and 36 decreased proteins. Moreover, 47 proteins were newly reported in PCOS. The alterations in the five significantly decreased proteins (EREG, inhibin βA, IDE, PDGF-D and KNG1) were further confirmed by ELISA and western blot. The level of these proteins were directly associated with the low progesterone, and the expression could be upregulated by progesterone. EREG and inhibin βA also promoted the proliferation and inhibited the apoptosis of ovarian granulosa cells. Conclusion: The study highlights that serum proteins are differentially expressed in PCOS patients and healthy women, and EREG and inhibin βA levels are upregulated by progesterone, which are correlated with ovarian functions. The study suggests that EREG and inhibin βA may be applied as novel potential biomarkers for PCOS with low progesterone level.

Transcription factor‑microRNA synergistic regulatory network revealing the mechanism of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is the most common type of endocrine disorder, affecting 5–11% of women of reproductive age worldwide. Transcription factors (TFs) and microRNAs are considered to have crucial roles in the developmental process of several diseases and have synergistic regulatory actions. However, the effects of TFs and microRNAs, and the patterns of their cooperation in the synergistic regulatory network of PCOS, remain to be elucidated. The present study aimed to determine the possible mechanism of PCOS, based on a TF-microRNA synergistic regulatory network. Initially, the differentially expressed genes (DEGs) in PCOS were identified using microarray data of the GSE34526 dataset. Subsequently, the TFs and microRNAs which regulated the DEGs of PCOS were identified, and a PCOS-associated TF-microRNA synergistic regulatory network was constructed. This network included 195 DEGs, 136 TFs and 283 microRNAs, and the DEGs were regulated by TFs and microRNAs. Based on topological and functional enrichment analyses, SP1, mir-355-5p and JUN were identified as potentially crucial regulators in the development of PCOS and in characterizing the regulatory mechanism. In conclusion, the TF-microRNA synergistic regulatory network constructed in the present study provides novel insight on the molecular mechanism of PCOS in the form of synergistic regulated model.

The correlation of plasma omentin-1 with insulin resistance in non-obese polycystic ovary syndrome

ObjectivesAberrant circulating adipokines are considered to be related to the pathological mechanism of polycystic ovary syndrome (PCOS). This study aims to evaluate the relationship between plasma omentin-1 levels, metabolic and hormonal parameters in the setting of non-obese Chinese women with PCOS. Material and methodsThis was a case-controlled, cross-sectional study of 153 non-obese (BMI<25kg/m2) PCOS and 114 age-matched healthy non-obese control individuals. Levels of plasma omentin-1, fasting blood glucose, insulin and sexual hormones and ovary volume were analyzed in all subjects. ResultsPlasma omentin-1 levels of non-obese PCOS individuals were significantly lower than in healthy non-obese controls. Body Mass Index (BMI), homeostasis model of assessment for insulin resistance index (HOMA-IR), levels of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), LH/FSH ratio and ovary volume (OV) were significantly higher in subjects with PCOS than controls. In the HOMA-IR stratified subgroups, PCOS individuals with insulin resistance had lower omentin-1 than those without insulin resistance after BMI adjustment. Omentin-1 was negatively correlated with BMI, HOMA-IR and fasting insulin. Multiple linear regressions revealed that BMI contributed to omentin-1 levels. Ovary volume was negatively correlated to HOMA-IR but had no correlation with omentin-1. ConclusionsPlasma omentin-1 concentrations were decreased in the non-obese PCOS group. Insulin resistance could further decrease plasma omentin-1 in non-obese individuals with PCOS independent of BMI status.

Studies on mechanism of polycystic ovary syndrome and the diagnosis and treatment princial for adolescents

Studies on mechanism of polycystic ovary syndrome and the diagnosis and treatment princial for adolescents