Polycystic ovary syndrome and adipose tissue |
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| Institution: | 1. CHU Lille, Department of Diabetology, Endocrinology, Metabolism and Nutrition, Lille University Hospital, 59000 Lille, France;2. Center for rare endocrine diseases of growth and development, ERN-HCP, Sorbonne University, Endocrinology, Diabetology and Reproductive Medicine, Saint-Antoine Hospital, AP-HP, 75012 Paris, France;3. CHU Brest, Department of Diabetology and Endocrinology, Brest University Hospital, 29200 Brest, France;1. Department of Endocrinology, Seth G S Medical College and KEM Hospital, 103, 1st floor, OPD building, KEM Hospital Campus, Parel, Mumbai, Maharashtra 400012, India;2. Department of Endocrinology, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, India;3. Jawaharlal Nehru Medical College, Karnataka, India;4. Department of Nephrology, Seth G S Medical College and KEM Hospital, Mumbai, Maharashtra, India;1. Service de Biochimie générale, Hôpital Necker-Enfants Malades, Assistance Publique des Hôpitaux de Paris, Paris, France;2. Service d’Endocrinologie, Hôpital Cochin-Port Royal, Assistance Publique des Hôpitaux de Paris, Paris, France;1. Department of Endocrinology and Metabolism, University of Health Sciences, Diskapi Yildirim Beyazit Training and Research Hospital, Ankara, Turkey;2. Department of General Surgery, University of Health Sciences, Diskapi Yildirim Beyazit Training and Research Hospital, Ankara, Turkey;1. Department of Radiology and Nuclear Medicine, Radboud University Medical Centre, Nijmegen, 6500 HB Nijmegen, The Netherlands;2. Department of Radiology (C2-P-117), Section of Nuclear Medicine, Leiden University Medical Center, 2300 RC Leiden, The Netherlands;3. Biomedical Photonic Imaging Group, University of Twente, 7500 AE Enschede, The Netherlands;4. Radiation Science & Technology, Delft University of Technology, Mekelweg 15, 2629 JB Delft, The Netherlands;5. Department of Radiology and Nuclear Medicine, Rijnstate, Hospital, 6800 TA Arnhem, The Netherlands;6. Department of Biomedical Sciences and Humanitas Clinical and Research Centre, Department of Nuclear Medicine, Humanitas University, via Rita Levi Montalcini 4, 20072 Pieve Emanuele (MI), Italy;1. Erciyes University Medical School Department of Internal Medicine, Kayseri, Turkey;2. Erciyes University Medical School Department of Endocrinology, Kayseri, Turkey;3. Yeditepe University Medical School Department of Endocrinology, ?stanbul, Turkey;1. Service d’endocrinologie diabétologie et médecine de la reproduction, centre constitutif des maladies endocriniennes rares de la croissance, hôpital Saint-Antoine, AP–HP, 75012 Paris, France;2. U.F. de génétique moléculaire, département de génétique médicale, Sorbonne Université, hôpital Trousseau, AP–HP, Paris, France;3. Inserm, Childhood genetic disorders, UMRS 933, Sorbonne Université, hôpital Trousseau, 75012 Paris, France;4. U.F. de génétique chromosomique, département de génétique médicale, Sorbonne Université, hôpital Trousseau, AP–HP, Paris, France |
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| Abstract: | Polycystic ovary syndrome (PCOS) is the most common endocrine metabolic disorder in women of reproductive age. Typically, it is associated with ovulatory dysfunction: dysovulation or anovulation, and symptoms of hyperandrogenism. It incurs risk of metabolic disorders such as diabetes, dyslipidemia and fatty liver. As a key endocrine organ in metabolic homeostasis, adipose tissue is often implicated in these complications. Studies of white adipose tissue (WAT) in PCOS have focused on the mechanism of insulin resistance in this tissue. Clinically, abnormalities in WAT distribution are seen, with decreased waist-to-hip ratio and increased ratio of adipose to lean mass. Such abnormalities are greater when total circulating androgens are elevated. At tissue level, white adipocyte hyperplasia occurs, along with infiltration of macrophages. Secretion of adipokines, cytokines and chemo-attractant proteins is increased in a pro-inflammatory manner, leading to reduced insulin sensitivity via alteration of glucose transporters, and hence decreased glucose uptake. The kinetics of non-esterified fatty acids (or free fatty acids) is also altered, leading to lipotoxicity. In recent years, brown adipose tissue (BAT) has been studied in women with PCOS. Although abundance is low in the body, BAT appears to play a significant role in energy expenditure and metabolic parameters. Both supra-clavicular skin temperature, which reflects BAT activity, and BAT mass are reduced in women with PCOS. Moreover, BAT mass and body mass index (BMI) are inversely correlated in patients. In the adipocyte, increased total circulating androgen levels reduce expression of uncoupling protein 1 (UCP1), a key protein in the brown adipocyte, leading to reduced biogenesis and mitochondrial respiration and hence a reduction in post-prandial thermogenesis. BAT is currently being investigated as a possible new therapeutic application. |
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| Keywords: | Polycystic ovary syndrome White adipose tissue Insulin resistance Brown adipose tissue |
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