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      Estrogen suppresses adipogenesis by inhibiting S100A16 expression

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          Abstract

          The aim of this study is to determine the effects of E 2 on metabolic syndrome and the molecular mechanisms involving S100A16. Ovariectomized (OVX) rat models and mouse embryonic fibroblasts cell models were used. E 2 loss in OVX rats induced body weight gain and central abdominal fat accumulation, which were ameliorated by E 2 treatment under chow and high-fat diet (HFD) conditions. E 2 decreased the expression of the adipocyte marker genes PPAR γ, aP2, C/EBP α, and S100A16. E 2 inhibited adipogenesis. Overexpression of S100A16 reversed the E 2-induced adipogenesis effect. A luciferase assay showed that E 2 inhibited the expression of S100A16. E 2 treatment decreased body weight gain and central abdominal fat accumulation under both chow and HFD conditions. Also, E 2 suppressed adipogenesis by inhibiting S100A16 expression.

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          The emergence of the metabolic syndrome with menopause.

          Molly C Carr (2003)
          Women with the metabolic syndrome (central obesity, insulin resistance, and dyslipidemia) are known to be at especially high risk for cardiovascular disease (CVD). The prevalence of the metabolic syndrome increases with menopause and may partially explain the apparent acceleration in CVD after menopause. The transition from pre- to postmenopause is associated with the emergence of many features of the metabolic syndrome, including 1) increased central (intraabdominal) body fat; 2) a shift toward a more atherogenic lipid profile, with increased low density lipoprotein and triglycerides levels, reduced high density lipoprotein, and small, dense low density lipoprotein particles; 3) and increased glucose and insulin levels. The emergence of these risk factors may be a direct result of ovarian failure or, alternatively, an indirect result of the metabolic consequences of central fat redistribution with estrogen deficiency. It is unclear whether the transition to menopause increases CVD risk in all women or only those who develop features of the metabolic syndrome. This article will review the features of the metabolic syndrome that emerge with estrogen deficiency. A better understanding of these metabolic changes with menopause will aid in the recognition and treatment of women at risk for future CVD, leading to appropriate interventions.
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            Plasma sex steroid hormones and risk of developing type 2 diabetes in women: a prospective study.

            JoAnn Manson, E Ding, N Rifai … (2007)
            Prospective data directly investigating the role of endogenous sex hormones in diabetes risk have been scant, particularly in women. We aimed to examine comprehensively plasma sex hormones in connection with risk of developing type 2 diabetes in postmenopausal women. We conducted a prospective, nested case-control study of plasma oestradiol, testosterone and dehydroepiandrosterone sulfate and risk of type 2 diabetes in a cohort of women health professionals with a mean age of 60.3 and 12.2 years since menopause. Among women not using hormone therapy and free of baseline cardiovascular disease, cancer and diabetes, 359 incident cases of type 2 diabetes were matched with 359 controls during an average follow-up of 10 years. Oestradiol and testosterone were each strongly and positively associated with risk of type 2 diabetes. After adjustment for BMI, family history, lifestyle and reproductive variables, the multivariable relative risks (95% CI) comparing the highest vs lowest quintile were 12.6 (2.83-56.3) for total oestradiol (p = 0.002 for trend), 13.1 (4.18-40.8) for free oestradiol (p < 0.001 for trend), 4.15 (1.21-14.2) for total testosterone (p = 0.019 for trend) and 14.8 (4.44-49.2) for free testosterone (p < 0.001 for trend). These associations remained robust after adjusting and accounting for other metabolic syndrome components and baseline HbA(1c) levels. In postmenopausal women, higher plasma levels of oestradiol and testosterone were strongly and prospectively related to increased risk of developing type 2 diabetes. These prospective data indicate that endogenous levels of sex hormones may play important roles in the pathogenesis of type 2 diabetes. ClinicalTrials.gov ID no.: NCT00000479.
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              AliBaba2: context specific identification of transcription factor binding sites.

              Niels Grabe (2001)
              Currently, prediction of transcription factor binding sites is widely done using matrices collected from literature. This leads to several problems. We cannot actively control the conservation of the matrices, we cannot systematically use all binding sites available, we do not know which sites were used and which were discarded in matrix construction, we cannot compare and evaluate matrices easily, we cannot detect redundancy and we cannot control sensitivity and specificity. So we are lacking control during the identification process. In this paper a method to overcome these problems is proposed. It is assumed that each binding site has an unknown context which determines its sequence. This leads to the idea of constructing specific matrices for each sequence we are analysing. To do so we have to regard identification of binding sites as a general process, starting at a dataset of known binding sites and ending with the identification of a potential new binding site. In this paper such a process is presented. Besides overcoming the mentioned problems, the implementation also reaches a significantly higher accuracy than current approaches. Evaluations are done analysing all binding sites of TRANSFAC 3.5 public. The resulting tool AliBaba2 is available at http://wwwiti.cs.uni-magdeburg.de/grabe/alibaba2.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Mol Endocrinol
                Journal ID (iso-abbrev): J. Mol. Endocrinol
                Journal ID (publisher-id): JME
                Title: Journal of Molecular Endocrinology
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Print): 0952-5041
                ISSN (Electronic): 1479-6813
                Publication date (Print): June 2014
                Publication date (Electronic preprint): 5 February 2014
                Volume: 52
                Issue: 3
                Pages: 235-244
                Affiliations
                [1 ]Department of Geratology The First Affiliated Hospital, Nanjing Medical University Nanjing, 210029China
                [2 ]Laboratory Animal Center, The First Affiliated Hospital, Nanjing Medical University Nanjing, 210029China
                [3 ]The Center of Metabolism, Nanjing Medical University Nanjing, 210029China
                [4 ]Department of Urology Zhongda Hospital Affiliated to Southeast University Nanjing, 210008China
                [5 ]Department of Orthopedics Jiangsu Province Hospital of TCM Affiliated Hospital of Nanjing University of TCM Nanjing, JiangsuChina
                [6 ]Department of Endocrinology Changzhou Wujin People's Hospital 213000, Changzhou, JiangsuChina
                Author notes
                Correspondence should be addressed to Y Liu; Email: liuyun@ 123456njmu.edu.cn
                Article
                Publisher ID: JME130273
                DOI: 10.1530/JME-13-0273
                PMC ID: 4045221
                PubMed ID: 24501224
                SO-VID: 3180af15-a1ef-46b3-a511-67a2783aa202
                Copyright © © 2013 The authors
                License:

                This work is licensed under a Creative Commons Attribution 3.0 Unported License

                History
                Date revision received : 31 January 2014
                Date accepted : 5 February 2014
                Categories
                Subject: Research

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: estrogen,metabolic syndrome,s100a16
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: estrogen, metabolic syndrome, s100a16

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