Plasma omentin and adiponectin levels as markers of adipose tissue dysfunction in normal weight and obese women with polycystic ovary syndrome

2014 ◽  
Vol 81 (4) ◽  
pp. 529-535 ◽  
Author(s):  
Bartłomiej Orlik ◽  
Paweł Madej ◽  
Aleksander Owczarek ◽  
Piotr Skałba ◽  
Jerzy Chudek ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Normal Weight ◽  
Obese Women ◽  
Ovary Syndrome ◽  
Adipose Tissue Dysfunction

scholarly journals The Altered Mononuclear Cell-Derived Cytokine Response to Glucose Ingestion Is Not Regulated by Excess Adiposity in Polycystic Ovary Syndrome

2014 ◽  
Vol 99 (11) ◽  
pp. E2244-E2251 ◽  
Author(s):  
Frank González ◽  
Chang Ling Sia ◽  
Marguerite K. Shepard ◽  
Neal S. Rote ◽  
Judi Minium
Keyword(s):  
Body Composition ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Normal Weight ◽  
Cytokine Release ◽  
Ovary Syndrome ◽  
Excess Adiposity ◽  
Glucose Ingestion

Context: Excess adipose tissue is a source of inflammation. Polycystic ovary syndrome (PCOS) is a proinflammatory state and is often associated with excess abdominal adiposity (AA) alone and/or frank obesity. Objective: To determine the effect of glucose ingestion on cytokine release from mononuclear cells (MNC) in women with PCOS with and without excess AA and/or obesity. Design: A cross-sectional study. Setting: Academic medical center. Patients: Twenty-three women with PCOS (seven normal weight with normal AA, eight normal weight with excess AA, eight obese) and 24 ovulatory controls (eight normal weight with normal AA, eight normal weight with excess AA, eight obese). Intervention: Three-hour 75-g oral glucose tolerance test (OGTT). Main Outcome Measures: Body composition was measured by dual energy x-ray absorptiometry. Insulin sensitivity was derived from the OGTT (ISOGTT). TNFα, IL-6, and IL-1β release was measured in supernatants of cultured MNC isolated from blood samples drawn while fasting and 2 hours after glucose ingestion. Results: Insulin sensitivity was lower in obese subjects regardless of PCOS status and in normal-weight women with PCOS compared with normal-weight controls regardless of body composition status. In response to glucose ingestion, MNC-derived TNFα, IL-6, and IL-1β release decreased in both normal-weight control groups but failed to suppress in either normal-weight PCOS group and in obese women regardless of PCOS status. For the combined groups, the cytokine responses were negatively correlated with insulin sensitivity and positively correlated with abdominal fat and androgens. Conclusions: Women with PCOS fail to suppress MNC-derived cytokine release in response to glucose ingestion, and this response is independent of excess adiposity. Nevertheless, a similar response is also a feature of obesity per se. Circulating MNC and excess adipose tissue are separate and distinct sources of inflammation in this population.

scholarly journals Insulin Resistance and Polycystic ovary Syndrome: A Review

2019 ◽  
Vol 9 (1-s) ◽  
pp. 433-436 ◽  
Author(s):  
Mudasir Maqbool ◽  
Mohmad Amin Dar ◽  
Imran Gani ◽  
Mohammad Ishaq Geer
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Cell Function ◽  
Polycystic Ovary ◽  
Hepatic Clearance ◽  
Normal Weight ◽  
Obese Women ◽  
Primary Defect ◽  
Ovary Syndrome ◽  
Insulin Metabolism

Polycystic Ovary Syndrome (PCOS) is the most common, yet complex, endocrine disorder affecting women in their reproductive years and is a leading cause of infertility. This disease appears to be multifactorial and polygenic in nature involving multisystem dysfunction, namely reproduction, endocrine and metabolic. Hyperandrogenism and insulin resistance appear to be central cause to the pathophysiology of the disease. The glucose and insulin metabolism pathways have been studied and debated to understand whether Insulin Resistance is due to a defect in insulin action or a primary defect in β-cell function or decreased hepatic clearance of insulin, or a combination of all these factors. Numerous studies have demonstrated that obese, normal weight and thin women with PCOS have a form of insulin resistance that is unique and intrinsic to the disorder. Moreover obese women with PCOS possess an additional burden of insulin resistance resulting from their excess adiposity. Hyperinsulinemia leads to increase in androgen production directly by acting as a co-gonadotropin, augmenting Luteinizing Hormone activity within the ovary, and indirectly by increasing serum LH pulse amplitude. Whereas Androgens may in turn contribute at least partially to the insulin resistance state linked with PCOS.  In this review, we will briefly study the role of insulin resistance in polycystic ovary syndrome. Keywords: Polycystic ovary syndrome, insulin resistance, Hyperandrogenism.

Adiposity and metabolic dysfunction in polycystic ovary syndrome

2015 ◽  
Vol 21 (2) ◽  
Author(s):  
Susan Sam
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Metabolic Disorders ◽  
Polycystic Ovary ◽  
Reproductive Age ◽  
Metabolic Dysfunction ◽  
Obese Women ◽  
Ovary Syndrome ◽  
Insulin Resistant

AbstractPolycystic ovary syndrome (PCOS) is the most common hormonal disorder among reproductive-age women and is associated with a high risk for metabolic disorders. Adiposity and insulin resistance are two prevalent conditions in PCOS and the likely culprits for the heightened metabolic risk. Up to 60% of women with PCOS are considered to be overweight or obese, and even among non-obese women with PCOS there is an increased accumulation of adipose tissue in abdominal depots. Insulin resistance in PCOS is unique and independent of obesity, as even non-obese women with this condition are frequently insulin resistant. However, obesity substantially aggravates the insulin resistance and the metabolic and reproductive abnormalities in women with PCOS. Recently, it has been shown that many aspects of adipose tissue function in PCOS are abnormal, and these abnormalities likely predispose to development of insulin resistance even in the absence of obesity. This review provides an overview of these abnormalities and their impact on development of metabolic disorders. At the end, an overview of the therapeutic options for management of adiposity and its complications in PCOS are discussed.

scholarly journals The clinical significance and primary determinants of hirsutism in patients with polycystic ovary syndrome

2013 ◽  
Vol 168 (6) ◽  
pp. 871-877 ◽  
Author(s):  
Dimitrios Panidis ◽  
Konstantinos Tziomalos ◽  
Efstathios Papadakis ◽  
Panagiotis Chatzis ◽  
Eleni A Kandaraki ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Polycystic Ovary Syndrome ◽  
Abdominal Obesity ◽  
Polycystic Ovary ◽  
Linear Regression Analysis ◽  
Serum Testosterone ◽  
Normal Weight ◽  
Binary Logistic Regression Analysis ◽  
Obese Women ◽  
Ovary Syndrome

ObjectiveHirsutism is frequently present in patients with polycystic ovary syndrome (PCOS) and is a major sign of hyperandrogenism. However, other disorders frequently present in PCOS, particularly abdominal obesity and insulin resistance (IR), have also been implicated in the development of hirsutism in this population but relevant data are limited. We aimed to define the determinants of the presence of hirsutism in PCOS.DesignObservational study.MethodsWe studied 1297 patients with PCOS (age 24.3±5.8 years, BMI 26.8±6.9 kg/m2). Hirsutism was defined as a modified Ferriman–Gallwey score ≥8.ResultsWomen with hirsutism were younger, had greater BMI, and had higher levels of circulating androgens than women without hirsutism; markers of IR did not differ between the two groups after adjustment for age and BMI. The prevalence of hirsutism progressively declined with age, was lower in normal-weight women than in overweight and obese women, and was comparably prevalent in the hyperandrogenemic phenotypes of PCOS. In binary logistic regression analysis, independent predictors of the presence of hirsutism were younger age, larger waist circumference (W), and higher serum testosterone levels. In stepwise linear regression analysis, the Ferriman–Gallwey score independently correlated with age, W, free androgen index, and serum Δ4-androstenedione and DHEAS levels.ConclusionsBesides hyperandrogenemia, abdominal obesity, and young age are independently associated with the presence of hirsutism. In contrast, the relationship between IR and hirsutism appears to be mediated by the more severe obesity of insulin-resistant patients with PCOS.

scholarly journals Visfatin and Resistin Serum Levels in Normal-Weight and Obese Women With Polycystic Ovary Syndrome

2014 ◽  
Vol 12 (3) ◽  
Author(s):  
Fatemeh Farshchian ◽  
Fahimeh Ramezani Tehrani ◽  
Houshang Amirrasouli ◽  
Hooman Rahimi Pour ◽  
Mehdi Hedayati ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Serum Levels ◽  
Normal Weight ◽  
Obese Women ◽  
Ovary Syndrome

Hypothalamic-Pituitary-Adrenocortical Axis Hypersensitivity and Glucocorticoid Receptor Expression and Function in Women with Polycystic Ovary Syndrome

2011 ◽  
Vol 119 (10) ◽  
pp. 636-643 ◽  
Author(s):  
D.Vojnović Milutinović ◽  
D. Macut ◽  
I. Božić ◽  
J. Nestorov ◽  
S. Damjanović ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Glucocorticoid Receptor ◽  
Hpa Axis ◽  
Protein Concentration ◽  
Polycystic Ovary ◽  
Normal Weight ◽  
Receptor Expression ◽  
Obese Women ◽  
Ovary Syndrome ◽  
And Function

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.

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