scholarly journals Low-Frequency Electro-Acupuncture and Physical Exercise Improve Metabolic Disturbances and Modulate Gene Expression in Adipose Tissue in Rats with Dihydrotestosterone-Induced Polycystic Ovary Syndrome

Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3559-3568 ◽  
Author(s):  
Louise Mannerås ◽  
Ingibjörg H. Jonsdottir ◽  
Agneta Holmäng ◽  
Malin Lönn ◽  
Elisabet Stener-Victorin
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Polycystic Ovary ◽  
Uncoupling Protein ◽  
Low Frequency ◽  
Uncoupling Protein 2 ◽  
Metabolic Disturbances ◽  
Ovary Syndrome ◽  
Adipose Tissue Gene Expression

Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder associated with ovulatory dysfunction, hyperandrogenism, abdominal obesity, and insulin resistance. Pharmacotherapy is often unsatisfactory. This study evaluates the effects of low-frequency electro-acupuncture (EA) and physical exercise on metabolic disturbances and adipose tissue mRNA expression of selected genes in a rat PCOS model characterized by insulin resistance and adiposity. Dihydrotestosterone (inducing PCOS) or vehicle (control) was administrated continuously, beginning before puberty. At age 10 wk, PCOS rats were randomly divided into three groups; PCOS, PCOS EA, and PCOS exercise. PCOS EA rats received 2-Hz EA (evoking muscle twitches) three times/wk during 4–5 wk. PCOS exercise rats had free access to a running wheel for 4–5 wk. EA and exercise improved insulin sensitivity, measured by clamp, in PCOS rats. Exercise also reduced adiposity, visceral adipocyte size, and plasma leptin. EA increased plasma IGF-I. Real-time RT-PCR revealed increased expression of leptin and IL-6 and decreased expression of uncoupling protein 2 in visceral adipose tissue of PCOS rats compared with controls. EA restored the expression of leptin and uncoupling protein 2, whereas exercise normalized adipose tissue leptin and IL-6 expression in PCOS rats. Thus, EA and exercise ameliorate insulin resistance in rats with PCOS. This effect may involve regulation of adipose tissue metabolism and production because EA and exercise each partly restore divergent adipose tissue gene expression associated with insulin resistance, obesity, and inflammation. In contrast to exercise, EA improves insulin sensitivity and modulates adipose tissue gene expression without influencing adipose tissue mass and cellularity.

scholarly journals Expression of the CD11c gene in subcutaneous adipose tissue is associated with cytokine level and insulin resistance in women with polycystic ovary syndrome

2012 ◽  
Vol 167 (5) ◽  
pp. 705-713 ◽  
Author(s):  
Tao Tao ◽  
Shengxian Li ◽  
Aimin Zhao ◽  
Yanyun Zhang ◽  
Wei Liu
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Subcutaneous Adipose Tissue ◽  
Polycystic Ovary ◽  
Mrna Abundance ◽  
Model Assessment ◽  
Ovary Syndrome ◽  
Subcutaneous Adipose

Objective Alterations in the phenotypes of macrophages in adipose tissue play a key role in inflammation and insulin resistance (IR). The phenotypes of macrophages in subcutaneous adipose tissue (SAT) and the relationship between proinflammation markers and IR in women with polycystic ovary syndrome (PCOS) remain unclear. The objectives of this study are to characterize the gene expression of macrophage markers and cytokines in the SAT of PCOS women and to estimate their relationships with circulating levels of cytokines and IR. Methods The cross-sectional study involves 16 PCOS women and 18 normal control women. Cytokines and macrophage markers in the circulation and SAT were determined using ELISA, quantitative PCR, or immunofluorescence staining. IR was estimated using the homeostasis model assessment (HOMA-IR). Results The gene expression levels of CD11c along with TNF α and leptin in SAT remained significantly higher in PCOS women than in normal women (P<0.05). However, no significant differences were found in CD68 mRNA expression in SAT between women with and without PCOS (P>0.05). Furthermore, CD11c mRNA abundance provided a stronger contribution to models predicting serum levels of TNFα (sTNFα) than did CD68 mRNA abundance. Lastly, increased sTNFα was associated with increased HOMA-IR in PCOS women, and this association was independent of both overall and visceral adiposity. Conclusion The high expression level of CD11c mRNA in SAT was proved to be an important feature in PCOS women. Furthermore, CD11c mRNA abundance made a stronger contribution to models predicting sTNFα in which existing proinflammatory properties might significantly contribute to the pathogenesis of IR in PCOS women.

Uncoupling protein 2 expression affects androgen synthesis in polycystic ovary syndrome

Endocrine ◽  
2012 ◽  
Vol 43 (3) ◽  
pp. 714-723 ◽  
Author(s):  
Yun Liu ◽  
Hong Jiang ◽  
Fu-Qi Xing ◽  
Wu-Jian Huang ◽  
Li-Hua Mao ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Ovary Syndrome ◽  
Androgen Synthesis

scholarly journals The role of uncoupling protein 2 in macrophages and its impact on obesity-induced adipose tissue inflammation and insulin resistance

2020 ◽  
Vol 295 (51) ◽  
pp. 17535-17548
Author(s):  
Xanthe A. M. H. van Dierendonck ◽  
Tiphaine Sancerni ◽  
Marie-Clotilde Alves-Guerra ◽  
Rinke Stienstra
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Macrophage Activation ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Obesity And Diabetes ◽  
Adipose Tissue Macrophages

The development of a chronic, low-grade inflammation originating from adipose tissue in obese subjects is widely recognized to induce insulin resistance, leading to the development of type 2 diabetes. The adipose tissue microenvironment drives specific metabolic reprogramming of adipose tissue macrophages, contributing to the induction of tissue inflammation. Uncoupling protein 2 (UCP2), a mitochondrial anion carrier, is thought to separately modulate inflammatory and metabolic processes in macrophages and is up-regulated in macrophages in the context of obesity and diabetes. Here, we investigate the role of UCP2 in macrophage activation in the context of obesity-induced adipose tissue inflammation and insulin resistance. Using a myeloid-specific knockout of UCP2 (Ucp2ΔLysM), we found that UCP2 deficiency significantly increases glycolysis and oxidative respiration, both unstimulated and after inflammatory conditions. Strikingly, fatty acid loading abolished the metabolic differences between Ucp2ΔLysM macrophages and their floxed controls. Furthermore, Ucp2ΔLysM macrophages show attenuated pro-inflammatory responses toward Toll-like receptor-2 and -4 stimulation. To test the relevance of macrophage-specific Ucp2 deletion in vivo, Ucp2ΔLysM and Ucp2fl/fl mice were rendered obese and insulin resistant through high-fat feeding. Although no differences in adipose tissue inflammation or insulin resistance was found between the two genotypes, adipose tissue macrophages isolated from diet-induced obese Ucp2ΔLysM mice showed decreased TNFα secretion after ex vivo lipopolysaccharide stimulation compared with their Ucp2fl/fl littermates. Together, these results demonstrate that although UCP2 regulates both metabolism and the inflammatory response of macrophages, its activity is not crucial in shaping macrophage activation in the adipose tissue during obesity-induced insulin resistance.

scholarly journals Uncoupling protein-2 (UCP2) gene expression in subcutaneous and omental adipose tissue of Asian Indians

Adipocyte ◽  
2012 ◽  
Vol 1 (2) ◽  
pp. 101-107 ◽  
Author(s):  
Sujata R. Mahadik ◽  
Ramchandra D. Lele ◽  
Dhananjaya Saranath ◽  
Anika Seth ◽  
Vikram Parikh
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Asian Indians ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Omental Adipose Tissue ◽  
Ucp2 Gene

scholarly journals The Polycystic Ovary Syndrome and the Metabolic Syndrome: A Possible Chronobiotic-Cytoprotective Adjuvant Therapy

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Eduardo Spinedi ◽  
Daniel P. Cardinali
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
White Adipose Tissue ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
The Metabolic Syndrome ◽  
Obstructive Sleep ◽  
The Impact

Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients’ treatment.

scholarly journals The conservative treatment in adolescents with the Polycystic ovary syndrome

2016 ◽  
Vol 11 (4) ◽  
pp. 337-341
Author(s):  
Adrian NEACȘU ◽  
◽  
Cătălina Diana STĂNICĂ ◽  
Constantin Dimitrie NANU ◽  
◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Lifestyle Modification ◽  
Polycystic Ovary ◽  
Obese Women ◽  
Metabolic Disturbances ◽  
Childbearing Age ◽  
Ovary Syndrome ◽  
Oral Antidiabetic Agents ◽  
Menstrual Cycles

Polycystic ovary syndrome (PCOS) is a common endocrine and heterogeneous dysfunction, characterized by chronic anovulation and androgen excess, affecting 6-10% of women of childbearing age. It is the most common cause of anovulatory infertility. It seems that the key element in the pathophysiology of PCOS is increased insulin resistance. The correction of infertility in teens is not a priority. They can receive treatment to normalize menstrual cycles, with the reduction of symptoms and improvement of metabolic disorders. Many overweight teens have increased insulinemia, which may play a role in the development of PCOS. Standard treatment is oral estroprogestative, used to perform regular menstrual cycles. Normalize menstrual cycles can be done with oral contraceptives or oral antidiabetic agents that improve metabolic dysfunctions. An adjuvant approach of the utmost importance for teens is lifestyle modification and diet. Teen treatment should be individualized depending on a number of peculiarities that have to be taken into account: menstruation disorders, mastopathies and ovarian dystrophies, hyperandrogenism syndrome, sexually transmitted diseases and other associated disorders. In obese women with PCOS, weight loss improves hyperandrogenism, reduces metabolic disturbances, reduces insulin resistance and insulinemia, improves fertility rate, stimulates ovulation.

scholarly journals Body Composition, Serum Concentrations of Androgens and Insulin Resistance in Different Polycystic Ovary Syndrome Phenotypes

2020 ◽  
Vol 9 (3) ◽  
pp. 732 ◽  
Author(s):  
Aleksandra Maria Polak ◽  
Agnieszka Adamska ◽  
Anna Krentowska ◽  
Agnieszka Łebkowska ◽  
Justyna Hryniewicka ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Composition ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Control Group ◽  
Model Assessment ◽  
Serum Concentrations ◽  
Metabolic Disturbances ◽  
Ovary Syndrome ◽  
G Ratio

Insulin resistance and hyperandrogenemia observed in polycystic ovary syndrome (PCOS) are associated with metabolic disturbances and could be connected with body composition pattern. To date, several studies defining the parameters of body composition using dual energy X-ray absorptiometry (DXA) method in the group of PCOS patients have been published, however, without the analysis in different phenotypes. The aim of the present study was to investigate the relationships between serum androgens concentration, insulin resistance and distribution of fat mass using DXA method in various PCOS phenotypes according to the Rotterdam criteria. We examined 146 women: 34 (38%) had PCOS phenotype A, 20 (23%) phenotype B, 20 (23%) phenotype C and 15 (16%) phenotype D (with mean age of each phenotype 25 years), and 57 control subjects (mean age of 25.5 years). Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Serum concentrations of testosterone, androstenedione and dehydroepiandrosterone sulfate (DHEA-S) were assessed and free androgen index (FAI) was calculated. In phenotypes A, B and C, we observed higher FAI in comparison to the control group (all p < 0.01). Serum concentrations of androstenedione and DHEA-S were higher in phenotypes A and C in comparison to the control group (all p < 0.01). However, only in phenotype A we found higher visceral adipose tissue (VAT) mass and android/gynoid ratio (A/G ratio) in comparison to the control group (all p < 0.01). In phenotype A, we observed connection of VAT with FAI (r = 0.58, p < 0.01). Accordingly, A/G ratio was related with FAI in all phenotypes (all p < 0.05). Additionally, in phenotype C, A/G ratio was related to serum concentrations of DHEA-S and androstenedione (r = 0.46, p = 0.03; r = 0.53, p = 0.01, respectively). We also found connections of HOMA-IR with VAT and A/G ratio in all phenotypes (all p < 0.05). Women with phenotype A had higher amount of VAT and A/G ratio in comparison to the control group. Serum concentration of androgens and insulin resistance are connected with VAT and A/G ratio in normoandrogenic and hyperandrogenic PCOS phenotypes.

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