Peri-muscular adipose tissue may play a unique role in determining insulin sensitivity/resistance in women with polycystic ovary syndrome

AbstractPolycystic ovary syndrome is a heterogeneous endocrine and metabolic disorder associated with abdominal obesity, dyslipidemia and insulin resistance. Since abdominal obesity is characterized by low-grade inflammation, the aim of the study was to investigate whether visceral adipose tissue inflammation linked to abdominal obesity and dyslipidemia could lead to impaired insulin sensitivity in the animal model of polycystic ovary syndrome.Female Wistar rats were treated with nonaromatizable 5α-dihydrotestosterone pellets in order to induce reproductive and metabolic characteristics of polycystic ovary syndrome. Glucose, triglycerides, non-esterified fatty acids and insulin were determined in blood plasma. Visceral adipose tissue inflammation was evaluated by the nuclear factor kappa B intracellular distribution, macrophage migration inhibitory factor protein level, as well as TNFα, IL6 and IL1β mRNA levels. Insulin sensitivity was assessed by intraperitoneal glucose tolerance test and homeostasis model assessment index, and through analysis of insulin signaling pathway in the visceral adipose tissue.Dihydrotestosterone treatment led to increased body weight, abdominal obesity and elevated triglycerides and non-esterified fatty acids, which were accompanied by the activation of nuclear factor kappa B and increase in macrophage migration inhibitory factor, IL6 and IL1β levels in the visceral adipose tissue. In parallel, insulin sensitivity was affected in 5α-dihydrotestosterone-treated animals only at the systemic and not at the level of visceral adipose tissue.The results showed that abdominal obesity and dyslipidemia in the animal model of polycystic ovary syndrome were accompanied with low-grade inflammation in the visceral adipose tissue. However, these metabolic disturbances did not result in decreased tissue insulin sensitivity.

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

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2014-2046 ◽

2014 ◽

Vol 99 (11) ◽

pp. E2244-E2251 ◽

Cited By ~ 16

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.

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Increase in subcutaneous adipose tissue and fat free mass in women with polycystic ovary syndrome is related to impaired insulin sensitivity

Gynecological Endocrinology ◽

10.3109/09513590.2012.708802 ◽

2012 ◽

Vol 29 (2) ◽

pp. 152-155 ◽

Cited By ~ 8

Author(s):

Aydogan Aydogdu ◽

Ilker Tasci ◽

Ozge Kucukerdonmez ◽

Serkan Tapan ◽

Sebnem Aydogdu ◽

...

Keyword(s):

Adipose Tissue ◽

Insulin Sensitivity ◽

Polycystic Ovary Syndrome ◽

Subcutaneous Adipose Tissue ◽

Polycystic Ovary ◽

Fat Free Mass ◽

Ovary Syndrome ◽

Impaired Insulin ◽

Subcutaneous Adipose

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Brown adipose tissue thermogenesis in women with polycystic ovary syndrome

Endocrine Abstracts ◽

10.1530/endoabs.49.gp135 ◽

2017 ◽

Cited By ~ 1

Author(s):

Soulmaz Shorakae ◽

Eveline Jona ◽

Courten Barbora de ◽

Gavin Lambert ◽

Elisabeth Lambert ◽

...

Keyword(s):

Adipose Tissue ◽

Polycystic Ovary Syndrome ◽

Brown Adipose Tissue ◽

Polycystic Ovary ◽

Ovary Syndrome ◽

Brown Adipose ◽

Brown Adipose Tissue Thermogenesis

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Indirect Predictors of Visceral Adipose Tissue in Women with Polycystic Ovary Syndrome: A Comparison of Methods

Nutrients ◽

10.3390/nu13082494 ◽

2021 ◽

Vol 13 (8) ◽

pp. 2494

Author(s):

Małgorzata Kałużna ◽

Magdalena Czlapka-Matyasik ◽

Aleksandra Bykowska-Derda ◽

Jerzy Moczko ◽

Marek Ruchala ◽

...

Keyword(s):

Adipose Tissue ◽

Polycystic Ovary Syndrome ◽

Visceral Adipose Tissue ◽

Polycystic Ovary ◽

Age Groups ◽

Ovary Syndrome ◽

Women Subjects ◽

Pcos Group ◽

Total Body ◽

Visceral Adipose

Visceral adipose tissue (VAT) accumulation, is a part of a polycystic ovary syndrome (PCOS) phenotype. Dual-energy x-ray absorptiometry (DXA) provides a gold standard measurement of VAT. This study aimed to compare ten different indirect methods of VAT estimation in PCOS women. The study included 154 PCOS and 68 age- and BMI-matched control women. Subjects were divided into age groups: 18–30 y.o. and 30–40 y.o. Analysis included: body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), waist/height 0.5 (WHT.5R), visceral adipose index (VAI), lipid accumulation product (LAP), and fat mass index (FMI). VAT accumulation, android-to-gynoid ratio (A/G), and total body fat (TBF) was measured by DXA. ROC analysis revealed that WHtR, WHT.5R, WC, BMI, and LAP demonstrated the highest predictive value in identifying VAT in the PCOS group. Lower cut-off values of BMI (23.43 kg/m2) and WHtR (0.45) were determined in the younger PCOS group and higher thresholds of WHtR (0.52) in the older PCOS group than commonly used. Measuring either: WHtR, WHT.5R, WC, BMI, or LAP, could help identify a subgroup of PCOS patients at high cardiometabolic risk. The current observations reinforce the importance of using special cut-offs to identify VAT, dependent on age and PCOS presence.

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