Inflammation and the Gut–Brain–Mood Connection (DRAFT)

2018 ◽  
Author(s):  
Katherine Falk ◽  
Barbara Bartlik ◽  
Janet Mindes
Keyword(s):  
Psychiatric Illness ◽  
Polycystic Ovary ◽  
The Body ◽  
Leaky Gut ◽  
Gut Permeability ◽  
Drinking Alcohol ◽  
Ovary Syndrome ◽  
Psychiatric Illnesses ◽  
Causative Factors ◽  
The Brain

Inflammation, oxidative stress, dysbiosis, and increased gut permeability (leaky gut) are now understood to be among the causative factors in depression, other psychiatric illnesses, and sexual dysfunction. This new appreciation of psychiatric illness as a systemic illness, occurring in the body as well as in the brain, offers new ways to understand and treat sexual problems such as polycystic ovary syndrome and erectile dysfunction. Leaky gut can be caused by medications such as antibiotics, NSAIDS, or aspirin; drinking alcohol; or the proinflammatory standard American diet. As conventional treatments for these conditions do not address sources of systemic inflammation, this integrative medicine approach is of great value for clinicians and can help relieve the suffering of patients and their loved ones.

scholarly journals Use of Inositols in Polycystic Ovary Syndrome

2020 ◽  
Vol 16 (28) ◽  
pp. 24-34
Author(s):  
O.A. Pustotina ◽  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Ovarian Function ◽  
Polycystic Ovary ◽  
The Body ◽  
Metabolic Parameters ◽  
Ovary Syndrome ◽  
Pathogenetic Role

The article presents key data on the physiology of inositols in the body, their pathogenetic role in the development of polycystic ovary syndrome, and the possibilities of myo-inositol and D-chiro-inositol in the restoration of ovarian function, metabolic parameters, and overcoming of infertility.

scholarly journals SAT-018 Androgen Actions in Adipose Tissue and the Brain Are Key Mediators in the Development of Polycystic Ovary Syndrome

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Madeleine J Cox ◽  
Melissa C Edwards ◽  
Ali Aflatounian ◽  
Valentina Rodriguez Paris ◽  
William L Ledger ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Mouse Model ◽  
Hepatic Steatosis ◽  
Polycystic Ovary ◽  
Reproductive Traits ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Adipocyte Hypertrophy ◽  
The Brain

Abstract Polycystic ovary syndrome (PCOS) is a complex disorder characterised by endocrine, reproductive and metabolic abnormalities. Despite PCOS being the most common endocrinopathy affecting women of reproductive age, its etiology is poorly understood so there is no cure and symptom-oriented treatment is suboptimal. Elucidation of the underlying mechanisms involved in the pathogenesis of PCOS would pave the way for the development of new interventions for PCOS. Hyperandrogenism is the most consistent feature observed in PCOS patients, and recently aberrant neuroendocrine signalling and adipose tissue function have been proposed as playing a pathogenic role in the development of experimental PCOS. To investigate the role of adipose tissue and the brain as potential key sites for androgen receptor (AR)-mediated development of PCOS, we combined an adipocyte and brain-specific ARKO knockout (AdBARKO) mouse model with a dihydrotestosterone (DHT)-induced mouse model of PCOS. Wildtype (WT) and AdBARKO prepubertal mice were implanted with a blank or DHT implant and examined after 12 weeks. In WT control females, DHT exposure induced the PCOS reproductive traits of cycle irregularity, ovulatory dysfunction and reduced follicle health. In contrast, these reproductive features of PCOS were absent in DHT-treated AdBARKO females. The PCOS metabolic characteristics of increased adiposity, adipocyte hypertrophy and hepatic steatosis were induced by DHT in WT females. Despite DHT treatment, AdBARKO females displayed normal white adipose tissue weight, and adipocyte hypertrophy and hepatic steatosis were not evident. However, as with WT mice, DHT treatment induced increased fasting glucose levels in AdBARKO females. These results demonstrate that adipose tissue and the brain are key loci for androgen-mediated actions involved in the developmental origins of PCOS. These findings support targeting adipocyte and neuroendocrine AR-driven pathways in the future development of novel therapeutic strategies for PCOS.

scholarly journals Hormone Imbalance in Women with Infertility Caused by Polycystic Ovary Syndrome: Is There a Connection with Body Mass Index?

2020 ◽  
Vol 8 (B) ◽  
pp. 731-737
Author(s):  
Mariya Khmil ◽  
Stephan Khmil ◽  
Mariya Marushchak
Keyword(s):  
Body Mass Index ◽  
Polycystic Ovary Syndrome ◽  
Body Mass ◽  
Polycystic Ovary ◽  
Reproductive Hormones ◽  
The Body ◽  
Control Group ◽  
Ovary Syndrome ◽  
Hormone Levels ◽  
Hormonal Imbalance

BACKGROUND: The most common cause of female infertility is ovulation disorders, and the most common non-ovulatory cause is polycystic ovary syndrome (PCOS). AIM: The aim of the study was to define the reproductive hormone levels in women with infertility due to PCOS, depending on the body mass index (BMI). PATIENTS AND METHODS: The present study involved 100 women aged 25–39 years with infertility due to PCOS (PCOS group) and 30 women of the same age with infertility due to tubal-peritoneal causes (control group). Infertility due to PCOS was diagnosed according to the Rotterdam criteria. Hormone levels (anti-Müllerian [AMH], follicle-stimulating [FSH], luteinizing [LH], prolactin, estradiol, and testosterone) in blood serum were determined by ELISA. RESULTS: We detected a correlation between BMI and sex hormone levels as well as LH/FSH ratio. Notably, the ratio of LH/FSH in women with PCOS was significantly different compared to the control group, while at the same time, PCOS was significantly more frequent in overweight and obese patients compared to those with normal BMI. For instance, the LH/FSH ratio was 30.35% higher in women with Class 2 obesity than in the group of women with normal weight. However, in women with both PCOS and Class 3 obesity, the LH/FSH ratio was the lowest among those with a BMI of 25.0-39.9. CONCLUSIONS: We found a hormonal imbalance in women with infertility caused by PCOS: Increased levels of AMH and LH, estradiol, and testosterone and decreased FSH levels. Analysis of the relationship between the concentration of reproductive hormones and BMI showed a weak inverse relationship between BMI with FSH levels, as well as a direct correlation with the levels of LH, prolactin, estradiol, and testosterone, and LH/FSH ratio. Thus, obesity exacerbates the hormonal imbalance in women with infertility caused by PCOS.

scholarly journals Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

2020 ◽  
Author(s):  
Zixuan Gao ◽  
Xiaochen Ma ◽  
Yuhang Ge ◽  
Lei Wang ◽  
Ping Fu ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Protective Effect ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Body Weight Gain ◽  
Neuroprotective Effect ◽  
The Body ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Gonadotrophin Releasing Hormone

Abstract The exact pathogenesis of polycystic ovary syndrome (PCOS), the most common neuroendocrine disorder in women of reproductive age, has not been fully elucidated. Recent studies suggested that chronic inflammation and neurotransmitter disorder involved in the progress of PCOS. Troxerutin, a natural flavonoid, was reported to possess neuroprotective effect in several disease models by inhibiting inflammation or enhancing neurotrophic factor. In this study, we investigated the possible protective effect and mechanism of troxerutin in a dihydrotestosterone (DHT)-induced rat model of PCOS. The PCOS rat models were treated with troxerutin at a dose of 150mg/kg or 300mg/kg for up to 4 weeks. Results showed that 300mg/kg troxerutin significantly decreased the body weight gain and improved the pathological changes of ovary induced by DHT. Meanwhile, the elevated gonadotrophin-releasing hormone (GnRH), gonadotrophin and testosterone in the serum of PCOS rats were reduced with the treatment of troxerutin. The expression of kisspeptin and NKB in arcuate nucleus and their receptors kiss1r and NK3r in GnRH positive neurons of median eminence were markedly decreased in troxerutin-treated rats. Of note, the GnRH inhibitory regulator GABA and stimulatory regulator glutamate were also restored to the normal level by troxerutin. The present study indicated that troxerutin may exhibit a protective effect in PCOS rat model via regulating neurotransmitter release.

scholarly journals Effects of GLP-1R agonist or co-cyprindiol, in combination with metformin, on polycystic ovary syndrome in overweight women: A Randomized Clinical Trial

2021 ◽  
Author(s):  
Mingyu Liao ◽  
Xing Li ◽  
Hao Zhang ◽  
Ling Zhou ◽  
Liu Shi ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Metabolic Disorders ◽  
Polycystic Ovary ◽  
Controlled Trial ◽  
Clinical Effectiveness ◽  
The Body ◽  
Polycystic Ovaries ◽  
Open Label ◽  
Ovary Syndrome ◽  
Inflammatory Parameters

Objective:Polycystic ovary syndrome (PCOS) is characterized by reproductive dysfunctions and metabolic disorders. This study aims to compare the therapeutic effectiveness of glucagon-like peptide-1 receptor agonist (GLP-1RA) + Metformin (Met) versus co-cyprindiol (cyproterone acetate/ethinylestradiol, CPA/EE) + Met in overweight PCOS women and identify potential biomarkers. Methods: In this prospective, open-label randomized controlled trial, we recruited 60 overweight PCOS women into two groups at a 1:1 ratio to receive CPA/EE (2 mg/day) + Met (1,500 mg/day) or GLP-1RA (liraglutide, 0.6-1.2 mg/day) + Met (1,500 mg/day) for 12 weeks. The clinical effectiveness and adverse effects were evaluated, followed by plasma proteomic analysis and verification of critical biomarkers by ELISA. Results: Both interventions improved menstrual cycle, polycystic ovaries, LH levels, and LH/FSH ratio; meanwhile reduced the body weight, BMI, HbA1c, FBG, OGTT-30 min insulin, IL-6 and TNF-α. Whereas, GLP-1RA + Met showed a more robust improvement on HbA1c, HOMA-IR, lipid profiles, inflammatory parameters, and ovulation. CPA/EE + Met was more effective in reducing hyperandrogenemia. Plasma proteomic analysis revealed that the interventions altered proteins involved in reactive oxygen species detoxification (PRDX6, GSTO1, GSTP1, GSTM2), platelet degranulation (FN1), and the immune response (SERPINB9). Conclusions: CPA/EE+Met or GLP-1RA + Met treatment improved reproductive functions and alleviated metabolic disorders in overweight PCOS women. GLP-1RA + Met had a superior improvement in metabolism and inflammation. The novel plasma biomarkers PRDX6, FN1, and SERPINB9, might be indicators and targets for PCOS treatment.

scholarly journals Mitochondrial DNA 4977 bp Deletion in Peripheral Blood Is Associated With Polycystic Ovary Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Mujin Ye ◽  
Bin Hu ◽  
Weihui Shi ◽  
Fei Guo ◽  
Chenming Xu ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Polycystic Ovary Syndrome ◽  
Peripheral Blood ◽  
Polycystic Ovary ◽  
Follicle Stimulating Hormone ◽  
The Body ◽  
Mtdna Copy Number ◽  
Ovary Syndrome ◽  
Linear Dose ◽  
Deletion Rate

BackgroundPolycystic ovary syndrome (PCOS) is a common endocrine disorder worldwide. We aimed to examine the associations of two mitochondrial DNA (mtDNA) biomarkers in the peripheral blood, mtDNA copy number (CN), and mtDNA4977 deletion rate (DR), with PCOS in a clinical setting.MethodsWe performed a study involving 263 women with PCOS and 326 age-matched controls between June 2015 and June 2019. The mtDNA CN and mtDNA4977 DR were measured using multiplex probe-based qPCR. The associations of the mtDNA CN and mtDNA4977 DR with the risk of PCOS were estimated using logistic regression.ResultsAnalysis of the associations between mtDNA biomarkers and PCOS indicate that the mtDNA CN (P = 0.003) and mtDNA4977 DR (P < 0.001) in PCOS patients were significantly higher than those in the controls. After adjusting for the body mass index, luteinizing hormone/follicle-stimulating hormone ratio, and testosterone level, only higher mtDNA4977 DR was associated with PCOS (odds ratio 1.053, 95% confidence interval 1.024 to 1.083; P < 0.001). The linear dose-response trends of the mtDNA4977 DR were also supported by the quartile analysis.ConclusionMultivariable models suggest that mtDNA4977 DR levels are strongly associated with PCOS and represent an independent risk factor for PCOS. Further investigation of the utility of mtDNA as a biomarker for PCOS is warranted.

M395 GENES RELATED TO GLYCOSYLATION IN THE BRAIN OF MICE WITH POLYCYSTIC OVARY SYNDROME TRANSPLANTED WITH ADIPOSE TISSUE

2012 ◽  
Vol 119 ◽  
pp. S658-S658
Author(s):  
M. de N.G. Ritto ◽  
C.F. Baptista ◽  
E.H.S. Freitas ◽  
S.M.R. de Noronha ◽  
S.A.A. Corrêa-Noronha ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
The Brain

scholarly journals Troxerutin protects against DHT-induced polycystic ovary syndrome in rats

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Zixuan Gao ◽  
Xiaochen Ma ◽  
Jing Liu ◽  
Yuhang Ge ◽  
Lei Wang ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Protective Effect ◽  
Rat Model ◽  
Polycystic Ovary ◽  
Body Weight Gain ◽  
Neuroprotective Effect ◽  
The Body ◽  
Reproductive Age ◽  
Ovary Syndrome ◽  
Gonadotrophin Releasing Hormone

AbstractThe exact pathogenesis of polycystic ovary syndrome (PCOS), the most common neuroendocrine disorder in women of reproductive age, has not been fully elucidated. Recent studies suggested that chronic inflammation and neurotransmitter disorder involved in the progress of PCOS. Troxerutin, a natural flavonoid, was reported to possess neuroprotective effect in several disease models by inhibiting inflammation or enhancing neurotrophic factor. In this study, we investigated the possible protective effect and mechanism of troxerutin in a dihydrotestosterone (DHT)-induced rat model of PCOS. The PCOS rat models were treated with troxerutin at a dose of 150 mg/kg or 300 mg/kg for up to 4 weeks. Results showed that 300 mg/kg troxerutin significantly decreased the body weight gain and improved the pathological changes of ovary induced by DHT. Meanwhile, the elevated gonadotrophin-releasing hormone (GnRH), gonadotrophin and testosterone in the serum of PCOS rats were reduced with the treatment of troxerutin. The expression of kisspeptin and NKB in arcuate nucleus and their receptors kiss1r and NK3r in GnRH positive neurons of median eminence were markedly decreased in troxerutin-treated rats. Of note, the GnRH inhibitory regulator GABA and stimulatory regulator glutamate were also restored to the normal level by troxerutin. The present study indicated that troxerutin may exhibit a protective effect in PCOS rat model via regulating neurotransmitter release.

scholarly journals Neuroendocrine Impairments of Polycystic Ovary Syndrome

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2230-2242 ◽  
Author(s):  
Amy Ruddenklau ◽  
Rebecca E Campbell
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Neuronal Network ◽  
Negative Feedback ◽  
Polycystic Ovary ◽  
Steroid Hormone ◽  
Unknown Etiology ◽  
Androgen Excess ◽  
Ovary Syndrome ◽  
The Brain

Abstract Polycystic ovary syndrome (PCOS) is a prevalent and distressing disorder of largely unknown etiology. Although PCOS defined by ovarian dysfunction, accumulating evidence supports a critical role for the brain in the ontogeny and pathophysiology of PCOS. A critical pathological feature of PCOS is impaired gonadal steroid hormone negative feedback to the GnRH neuronal network in the brain that regulates fertility. This impairment is associated with androgen excess, a cardinal feature of PCOS. Impaired steroid hormone feedback to GnRH neurons is thought to drive hyperactivity of the neuroendocrine axis controlling fertility, leading to a vicious cycle of androgen excess and reproductive dysfunction. Decades of clinical research have been unable to uncover the mechanisms underlying this impairment, because of the extreme difficulty in studying the brain in humans. It is only recently, with the development of preclinical models of PCOS, that we have begun to unravel the role of the brain in the development and progression of PCOS. Here, we provide a succinct overview of what is known about alterations in the steroid hormone–sensitive GnRH neuronal network that may underlie the neuroendocrine defects in clinical PCOS, with a particular focus on those that may contribute to impaired progesterone negative feedback, and the likely role of androgens in driving this impairment.

Sign in / Sign up

Export Citation Format

Share Document