Effect of Acupuncture on Ovary Morphology and Function in DHEA-Induced Polycystic Ovary Syndrome Model Rats

2021 ◽  
Vol 27 (3) ◽  
pp. 220-224
Author(s):  
Dan Li ◽  
Peng Bai ◽  
Jin-yang Wu ◽  
Min Xie ◽  
Rui-zhen Zhao ◽  
...  
2020 ◽  
Author(s):  
Zheng Yanhua ◽  
Ying Xu ◽  
Hongxia Ma ◽  
Chengjie Liang ◽  
Tong Yang

Abstract Background: Etiology of polycystic ovary syndrome (PCOS) is unclear. Recent reports indicated that gut microbiota regulates metabolism and plays a major role in the development of PCOS.Methods: We used dihydrotestosterone (DHT) or letrozole (LET) to induce PCOS model rat. At the end of the experiment, ovarian morphology, hormonal and metabolic status were investigated in all rats. The molecular ecology of the fecal gut microbiota was analyzed by 16S rDNA high-throughput sequencing.Result: Rats induced by letrozole exhibited endocrine and reproductive characteristics, such as hyperandrogenism, abnormal oestrus cycles or complete acyclic, polycystic ovaries, and obesity. DHT-induced rats were showed obesity, irregular oestrus cycles, polycystic ovaries, lower level of HDL-C and lower activity of SOD than controls. Our study found that DHT can reduce the microbial richness in rats. PCoA plots confirmed that DHT group was statistically significantly separated from C group and LET group. LEfSe analysis showed that the family of Bacteroidales_S24_7_group, and genus Peptococcus and Turicibacter may play vital roles in the health and function of control group. Genus of Bifidobacteriales and Vibro may play roles in the letrozole induced PCOS rats. And genus of Lachnospiraceae_NK4A136_group, Ruminococcus_1, Ruminiclostridium, Treponema_2, Anaerotruncus, Acetatifactor and Anaeroplasma may play vital roles in the intestine of DHT induced PCOS rats.Conclusion: DHT affected the composition and diversity of gut microbial community, and leads to the gut dysbiosis. Letrozole may benefit to the gut microbiome in some aspects, but it also may have a trend of inhibiting the expression of some anti-inflammatory genera in intestinal tract.


2011 ◽  
Vol 119 (10) ◽  
pp. 636-643 ◽  
Author(s):  
D.Vojnović Milutinović ◽  
D. Macut ◽  
I. Božić ◽  
J. Nestorov ◽  
S. Damjanović ◽  
...  

AbstractMolecular mechanisms underlying pathophysiology of polycystic ovary syndrome (PCOS), especially those related to cortisol signaling, are poorly understood. We hypothesized that modulation of glucocorticoid receptor (GR) expression and function, may underlie possible PCOS-related impairment of feedback inhibition of hypothalamic-pituitary-adrenocortical (HPA) axis activity and thus contribute to increased adrenal androgen production in women with PCOS.24 normal-weight and 31 obese women with PCOS were compared to 25 normal-weight controls. Fasting blood samples were collected for measurements of serum concentrations of dehydroepiandrosterone sulfate, testosterone, sex hormone-binding globulin, insulin, basal cortisol and cortisol after oral administration of 0.5 mg dexamethasone. Concentrations of GR mRNA, GR protein, mineralocorticoid receptor (MR) protein and heat shock proteins (Hsps), as well as the number of GR per cell (Bmax) and its equilibrium dissociation constant (KD) were measured in isolated peripheral blood mononuclear cells.An increase in HPA axis sensitivity to dexamethasone, an elevation of the GR protein concentration, and unaltered receptor functional status were found in both normal-weight and obese women with PCOS vs. healthy controls. Lymphocyte MR, Hsp90 and Hsp70 concentrations, and MR/GR ratio were similar in all groups. Correlation between Bmax and KD was weaker in the group of obese women with PCOS than in the other 2 groups.The results did not confirm the initial hypothesis, but imply that PCOS is associated with increased GR protein concentration and HPA axis sensitivity to dexamethasone.


2005 ◽  
Vol 152 (3) ◽  
pp. 389-394 ◽  
Author(s):  
E Carmina ◽  
F Orio ◽  
S Palomba ◽  
T Cascella ◽  
R A Longo ◽  
...  

Background: Adipocytokines are produced by adipose tissue and have been thought to be related to insulin resistance and other health consequences. We measured leptin, adiponectin, and resistin simultaneously in women with polycystic ovary syndrome (PCOS) and age- and weight-matched controls. Our hypothesis was that these simultaneous measurements would help determine whether adipocytokine secretion is abnormal in PCOS independent of body mass and whether these levels are related to insulin resistance as well as other hormonal changes. Methods: Fifty-two women with PCOS and 45 normal ovulatory women who were age- and weight-matched were studied. Blood was obtained for adipocytokines (leptin, adiponectin, and resistin) as well as hormonal parameters and markers of insulin resistance as assessed by the quantitative insulin-sensitivity check index. Body mass index (BMI) was stratified into obese, overweight, and normal subgroups for comparisons between PCOS and controls. Results: Adiponectin was lower (P < 0.05) and resistin was higher (P < 0.05) while leptin was similar to matched controls. Breakdown of the groups into subgroups showed a strong body mass relationship for leptin with no changes in resistin although adiponectin was lower in PCOS, even controlling for BMI. In controls, leptin and adiponectin and leptin and resistin correlated (P < 0.05) but not in PCOS. In controls, all adipocytokines correlated with markers of insulin resistance but not in PCOS. Conclusions: When matched for BMI status, decreased adiponectin in PCOS represent the most marked change. This alteration may be the result of altered adipose tissue distribution and function in PCOS but no correlation with insulin resistance was found.


2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Qi Xie ◽  
XingLiang Xiong ◽  
Na Xiao ◽  
Ke He ◽  
Maosheng Chen ◽  
...  

Polycystic ovary syndrome (PCOS) is the most common cause of anovulatory infertility in women of reproductive age. Chronic inflammation is considered to be the cause of ovarian dysfunction. Increasing evidence in animal studies and in preliminary clinical trials has demonstrated that MSCs possess immunomodulatory effects via their interaction with immune cells. However, their contribution to PCOS remains unclear. In this study, we showed that the administration of hUC-MSCs could efficiently improve the pathological changes of PCOS mice induced by dehydroepiandrosterone (DHEA), including ovarian histopathology and function. Moreover, we found that the administration of MSCs significantly downregulated the expression of proinflammatory factors (TNF-α, IL-1β, and IFN-γ) and fibrosis-related genes (CTGF) in ovarian and uterus tissues and affected the systemic inflammatory response. The percentage of peripheral neutrophils, M1 macrophages, and B cells was significantly reduced, while M2 macrophages and regulatory T cells (Tregs) were increased in hUC-MSC-treated mice. In the spleen, the percentage of neutrophils, M1 macrophages, IFN-γ+CD19+B cell, IFN-γ+CD4+T cells (Th1), and IL-17+CD4+T cells (Th17) was significantly decreased in hUC-MSC-treated mice. These results suggested that hUC-MSC treatment could alleviate ovarian dysfunction by inhibiting ovarian local and systemic inflammatory responses.


2021 ◽  
Vol 8 (4) ◽  
pp. 248-254
Author(s):  
Barnali Ray Basu ◽  
Sanchari Chakraborty ◽  
Ankita Samaddar ◽  
Nilansu Das ◽  
Sudip Kumar Saha

Polycystic ovary syndrome (PCOS), a multifaceted condition, often has salient features like insulin resistance (IR). Abnormal alternation in insulin synthesis and function usually alters PCOS expressivity by deviating molecular and biochemical activity underlying this pathophysiology.This review intends to unveil the molecular basis of the genetic polymorphism of IR and its correlation with PCOS. It also highlights the existing methods of IR estimation. Searching of different articles using keywords including PCOS, IR, and polymorphism in various databases was performed to illustrate the review article.POCS, and IR are complex and multifactorial conditions in terms of the contributing factors, their interactions, and expressivity. Further studies on diversified genotype responses to environmental and ethnic variances are required for precise understanding.Insulin resistance (IR) and polycystic ovary syndrome (PCOS) are intricately interacted conditions that abnormally alter functions from genetic to organ system level. Complex gene-environment interactions make it difficult to understand the etiology and manifestation, and so diagnosis and management approaches of the heterogeneous pathophysiology are not foolproof. Further studies on genetic susceptibility related to ethnic distribution are essential for the implementation of personalized treatment of IR and PCOS.


2016 ◽  
Vol 66 (1) ◽  
Author(s):  
Francesco Orio ◽  
Teresa Cascella ◽  
Francesco Giallauria ◽  
Stefano Palomba ◽  
Anna De Lorenzo ◽  
...  

Polycystic ovary syndrome (PCOS) is a good example of obesity-related cardiovascular complication affecting young women. PCOS is not only considered a reproductive problem but rather represents a complex endocrine, multifaceted syndrome with important health implications. Several evidences suggest an increased cardiovascular risk of cardiovascular disease associated with this syndrome, characterized by an impairment of heart structure and function, endothelial dysfunction and lipid abnormalities. All these features, probably linked to insulin-resistance, are often present in obese PCOS patients. Cardiovascular abnormalities represent important long-term sequelae of PCOS that need further investigations.


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