A Cross-Sectional Study of Alzheimer-Related Proteins in Women with Polycystic Ovary Syndrome
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Polycystic ovary syndrome (PCOS) is the most common endocrine condition in women of reproductive age, and several risk factors found in PCOS are associated with an increased risk of Alzheimer’s disease (AD). Proteins increased in AD have been reported to include fibronectin (FN) fragments 3 and 4 (FN1.3 and FN1.4, respectively) and ApoE. We hypothesized that Alzheimer-related proteins would be dysregulated in PCOS because of associated insulin resistance and obesity. In this comparative cross-sectional analysis, aptamer-based SomaScan proteomic analysis for the detection of plasma Alzheimer-related proteins was undertaken in a PCOS biobank of 143 women with PCOS and 97 control women. Amyloid precursor protein (APP) (p < 0.05) and amyloid P-component (APCS) (p < 0.001) were elevated in PCOS, while alpha-synuclein (SNCA) (p < 0.05) was reduced in PCOS. Associations with protective heat shock proteins (HSPs) showed that SNCA positively correlated with HSP90 (p < 0.0001) and HSP60 (p < 0.0001) in both the PCOS and control women. Correlations with markers of inflammation showed that APCS correlated with interleukin 6 (IL6) (p = 0.04), while Apolipoprotein (Apo) E3 correlated with TNF-alpha (p = 0.02). FN, FN1.3, FN1.4 and ApoE were all elevated significantly (p < 0.05). An AD-associated protein pattern with elevated FN, FN1.3, FN1.4 and ApoE was found in PCOS, in addition to elevated APP and reduced SNCA, which was the same as reported for type 2 diabetes (T2D) with, additionally, an elevation in APCS. With the AD biomarker pattern in PCOS being very similar to that in T2D, where there is an association between AD and T2D, this suggests that larger prospective cohort studies are needed in women with PCOS to determine if there is a causal association with AD.SUMMARY OBJECTIVE: Polycystic ovary syndrome can be divided into different subtypes, including insulin resistance and hyperandrogenism. The aim of this study was to investigate the relationship between serum asprosin levels and polycystic ovary syndrome subtypes. METHODS: A total of 93 women with polycystic ovary syndrome and 77 healthy women as controls were selected for this study. The clinical and laboratory data were compared between the Polycystic ovary syndrome group and the control group. The Polycystic ovary syndrome group was further divided into subgroups: (1) women with or without hyperandrogenism (polycystic ovary syndrome hyperandrogenism and Polycystic ovary syndrome none-hyperandrogenism, respectively) and (2) women with or without insulin resistance (polycystic ovary syndrome insulin resistance and Polycystic ovary syndrome none-insulin resistance, respectively). Serum asprosin was measured by using enenzyme-linked immunosorbent assay. RESULTS: Serum asprosin levels showed no significant difference between the polycystic ovary syndrome and control groups. However, it was significantly lower in the Polycystic ovary syndrome HA and insulin resistance groups compared with the respective Polycystic ovary syndrome none-hyperandrogenism and none-insulin resistance groups (p<0.05). In the Polycystic ovary syndrome group, serum asprosin was negatively correlated with body mass index, luteinizing hormone, testosterone, basal antral follicles, fasting insulin, homeostatic model assessment of insulin resistance, and triglycerides. After adjusting for body mass index, the correlations were not significant, and asprosin was only positively correlated with prolactin (prolactin; r=0.426, p<0.001). CONCLUSION: Our study shows that women with polycystic ovary syndrome hyperandrogenism or insulin resistance exhibit significantly lower serum asprosin levels compared with controls, and the lower asprosin level directly correlated with prolactin level.
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Polycystic ovary syndrome is a metabolic disease(PCOS).Most patients have insulin resistance(IR) in PCOS.Insulin resistance is the pathophysiological basis of PCOS.Its mechanisms including obesity and PCOS itself.Patients have insulin resistance in any body weight.PCOS involving IR in insulin regulation of glucose metabolism in multiple organs and links.Ovary have IR too.Lifestyle changes,weight control and the use of insulin sensitizer in patients with polycystic ovary syndrome are the important therapeutic measures of IR.
Carbohydrate Metabolism
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Acute‐phase serum amyloid A (A‐SAA) was shown recently to correlate with obesity and insulin resistance in humans. However, the mechanisms linking obesity‐associated inflammation and elevated plasma A‐SAA to insulin resistance are poorly understood. Using high‐fat diet‐ (HFD‐) fed mice, we found that plasma A‐SAA was increased early upon HFD feeding and was tightly associated with systemic insulin resistance. Plasma A‐SAA elevation was due to induction of Saa1 and Saa2 expression in liver but not in adipose tissue. In adipose tissue Saa3 was the predominant isoform and the earliest inflammatory marker induced, suggesting it is important for initiation of adipose tissue inflammation. To assess the potential impact of A‐SAA on adipose tissue insulin resistance, we treated 3T3‐L1 adipocytes with recombinant A‐SAA. Intriguingly, physiological levels of A‐SAA caused alterations in gene expression closely resembling those observed in HFD‐fed mice. Proinflammatory genes ( Ccl2, Saa3 ) were induced while genes critical for insulin sensitivity ( Irs1, Adipoq, Glut4 ) were down‐regulated. Our data identify HFD‐fed mice as a suitable model to study A‐SAA as a biomarker and a novel possible mediator of insulin resistance.
Amyloid (mycology)
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Objective To investigate the features of obesity and insulin resistance in polycystic ovary syndrome patients,and to analyze the relation of these clinical parameters to biochemical features.Methods Two hundred and seventy-six polycystic ovary syndrome patients were divided into obese group and no-obese group.The level of blood sugar and insulin,area under curve of insulin,the length of menses were compared between obese group and no-obese group.The relation of area under curve of insulin to biochemical features was analyzed.Results(1) Insulin resistance and the impaired glucose tolerance were not always congruity.(2) Compared with polycystic ovary syndrome patients without obese,the rate of insulin resistance was significantly higher in obese polycystic ovary syndrome patients(P0.05),and the length of menses was longer in obese polycystic ovary syndrome patients.(3) Insulin area under the curve was positively correlated with BMI and T,negatively correlated with ratio of LH/FSH.Conclusion Insulin resistance is common in polycystic ovary syndrome patients.Compared with polycystic ovary syndrome patients without obese,the rate of insulin resistance is significantly higher in obese group(P0.05).Obesity is an important risk factor for polycystic ovary syndrome patients,and it can aggravate the clinical signs of polycystic ovary syndrome.
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Androgen Excess
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Insulin resistance 'and polycystic ovary syndrome (PCOS) ': Part 1. The impact of insulin resistance
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in females of reproductive age with a prevalence of up to 20%. It is a multifactorial complex reproductive, endocrine, metabolic and psychological condition with insulin resistance playing a major role in its pathogenesis. Women with PCOS have a higher risk of cardiometabolic conditions. Insulin resistance has been implicated in numerous health conditions, such as cardiometabolic syndrome and PCOS.
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Introduction: Polycystic ovary syndrome is characterized by ovulatory dysfunction and hyperandrogenism. Although insulin resistance is not a diagnostic criterion for polycystic ovary syndrome, it has an important role in the development of the clinical presentation in a majority of patients with this syndrome. Many studies have examined the relationship of epicardial fat thickness with insulin resistance and cardiovascular complications. This study aimed to determine the relationship of epicardial fat thickness with polycystic ovary syndrome and insulin resistance. Methods: This cross-sectional study recruited women with polycystic ovary syndrome presenting to endocrinology clinic in Kermanshah city. Sixty-four patients with polycystic ovary syndrome, without underlying diseases, were divided into two groups of 32 according to the HOMA-IR index as insulin resistant and insulin sensitive. Their epicardial fat thickness was measured by transtorasic echocardiography. Results: The results of this study suggest that epicardial fat thickness has a direct and significant relationship with insulin resistance and BMI in patients with polycystic ovary syndrome. Conclusion: According to the results, the increase in the thickness of epicardial fat is independent of the disease in patients with polycystic ovary syndrome. The cause of the increased thickness is the metabolic syndrome and increased insulin resistance in these patients.
Hyperandrogenism
Polycystic ovarian disease
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Hyperinsulinemia
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Purpose of review As the prevalence of pediatric obesity escalates, polycystic ovary syndrome is an increasingly common morbidity for adolescent females. This review describes recent insights into the pathophysiology and treatment of polycystic ovary syndrome, with special attention given to the relationship between polycystic ovary syndrome and obesity. Recent findings Recent research has elucidated three key concepts in our understanding of polycystic ovary syndrome. First, patients may enter the hyperandrogenism–hyperinsulinism cycle of polycystic ovary syndrome via several pathways, including genetic polymorphisms that affect androgen synthesis, fetal programming that alters lipid and glucose metabolism, and obesity accompanied by insulin resistance. Second, obesity plays a significant role in the pathophysiology of polycystic ovary syndrome by increasing free androgen concentrations through multiple mechanisms. Finally, just as the etiology of polycystic ovary syndrome is multifactorial, successful treatment will probably require a combination of lifestyle modification and therapeutic interventions. Summary Obesity contributes to the pathophysiology of polycystic ovary syndrome and increases the likelihood of associated metabolic and cardiovascular morbidities.
Hyperandrogenism
Androgen Excess
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The etiology and pathogenesis of polycystic ovary syndrome (PCOS) is still unknown. Using real-time PCR, we detected that polycystic ovaries showed almost ten times lower expression of ghrelin mRNA than normal ovaries, whereas the mRNA levels in blood cells were similar in both study groups. This suggests that the presence of ghrelin in PCOS and normal ovaries may have an autocrine/paracrine modulatory effect on ovary functions and local significance in the etiology of PCOS.
Etiology
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