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      Sex-dependent Depot Differences in Adipose Tissue Development and Function; Role of Sex Steroids

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          Abstract

          Men and women are different in their fat mass and distribution pattern. The gynoid-type fat distribution, accumulation in lower-body, is considered to be protective while the android-type accumulation in upper-body, both in abdominal subcutaneous and visceral depots, is detrimental. Sex-dependent depot differences in adipose metabolic and endocrine functions are thought to contribute to the sexual disparity in fat distribution as well as its association with cardiometabolic risks. Although molecular details have not been completely elucidated, available evidence shows that sex steroid hormones are important factors governing sexual dimorphism in adipose tissue distribution and hence, risks for metabolic diseases. We will review sex-dependent heterogeneities in adipose tissue properties that can link their depot-specific biology to metabolic complications in men and women. In addition, we will also review how sex steroids regulate adipose tissue biology, both development and functional characteristics, with emphasis on their depot-dependent actions.

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          Increased visceral fat and decreased energy expenditure during the menopausal transition.

          J C Lovejoy, C Champagne, L. de Jonge … (2008)
          This study assessed longitudinal changes in body composition, fat distribution and energy balance in perimenopausal women. We hypothesized that total fat and abdominal body fat would increase at menopause due to decreased energy expenditure (EE) and declining estrogen, respectively. Observational, longitudinal study with annual measurements for 4 years. Healthy women (103 Caucasian; 53 African-American), initially premenopausal. During follow-up, lack of menstruation for 1 year and follicle-stimulating hormone >30 mIU ml(-1) defined a subject as postmenopausal. Fat and lean mass (dual-energy X-ray absorptiometry), visceral (VAT) and subcutaneous abdominal fat (SAT) (computed tomography), dietary intake (4-day food record), serum sex hormones and physical activity (tri-axial accelerometry). Twenty-four hour EE was measured by whole-room calorimeter in a subset of 34 women at baseline and at year 4. Body fat and weight increased significantly over time only in those women who became postmenopausal by year 4 (n=51). All women gained SAT over time; however, only those who became postmenopausal had a significant increase in VAT. The postmenopausal group also exhibited a significant decrease in serum estradiol. Physical activity decreased significantly 2 years before menopause and remained low. Dietary energy, protein, carbohydrate and fiber intake were significantly higher 3-4 years before the onset of menopause compared with menopause onset. Twenty-four hour EE and sleeping EE decreased significantly with age; however, the decrease in sleeping EE was 1.5-fold greater in women who became postmenopausal compared with premenopausal controls (-7.9 vs -5.3%). Fat oxidation decreased by 32% in women who became postmenopausal (P<0.05), but did not change in those who remained premenopausal. Middle-aged women gained SAT with age, whereas menopause per se was associated with an increase in total body fat and VAT. Menopause onset is associated with decreased EE and fat oxidation that can predispose to obesity if lifestyle changes are not made.
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            Overweight, obesity and central obesity in women with polycystic ovary syndrome: a systematic review and meta-analysis.

            S Lim, M. Davies, R Norman … (2012)
            BACKGROUND Polycystic ovary syndrome (PCOS) is closely associated with obesity but the prevalence of obesity varies between published studies. The objective of this research was to describe the prevalence of overweight, obesity and central obesity in women with and without PCOS and to assess the confounding effect of ethnicity, geographic regions and the diagnostic criteria of PCOS on the prevalence. METHODS MEDLINE, EMBASE, CINAHL, Cochrane Central Register of Controlled Trials (CENTRAL) and PSYCINFO were searched for studies reporting the prevalence of overweight, obesity or central obesity in women with and without PCOS. Data were presented as prevalence (%) and risk ratio (RR) [95% confidence interval (CI)]. Random-effect models were used to calculate pooled RR. RESULTS This systematic review included 106 studies while the meta-analysis included 35 studies (15129 women). Women with PCOS had increased prevalence of overweight [RR (95% CI): 1.95 (1.52, 2.50)], obesity [2.77 (1.88, 4.10)] and central obesity [1.73 (1.31, 2.30)] compared with women without PCOS. The Caucasian women with PCOS had a greater increase in obesity prevalence than the Asian women with PCOS compared with women without PCOS [10.79 (5.36, 21.70) versus 2.31 (1.33, 4.00), P < 0.001 between subgroups). CONCLUSIONS Women with PCOS had a greater risk of overweight, obesity and central obesity. Although our findings support a positive association between obesity and PCOS, our conclusions are limited by the significant heterogeneity between studies and further studies are now required to determine the source of this heterogeneity. Clinical management of PCOS should include the prevention and management of overweight and obesity.
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              Meta-analysis: effect of hormone-replacement therapy on components of the metabolic syndrome in postmenopausal women.

              E. Salpeter, Christine S. Walsh, E Greyber … (2006)
              To quantify the effects of hormone-replacement therapy (HRT) on components of the metabolic syndrome in postmenopausal women. Comprehensive searches of electronic databases were performed from April 1966 to October 2004. We included randomized controlled trials that were of at least 8 weeks duration and evaluated the effect of HRT on metabolic, inflammatory or thrombotic components. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Subgroup analysis evaluated the effects for transdermal and oral treatment and for diabetic and non-diabetic women. Pooled results of 107 trials showed that HRT reduced abdominal fat [-6.8% (CI, -11.8 to -1.9%)], HOMA-IR [-12.9% (CI, -17.1 to -8.6%)] and new-onset diabetes [relative risk 0.7 (CI, 0.6-0.9)] in women without diabetes. In women with diabetes, HRT reduced fasting glucose [-11.5% (CI, -18.0 to -5.1%)] and HOMA-IR [-35.8% (CI, -51.7 to -19.8%)]. HRT also reduced low-density lipoprotein/high-density lipoprotein cholesterol ratio [-15.7% (CI, -18.0 to -13.5%)], lipoprotein(a) [Lp(a)] [-25.0% [CI, -32.9 to -17.1%)], mean blood pressure [-1.7% (CI, -2.9 to -0.5%)], E-selectin [-17.3% (CI, -22.4 to -12.1%)], fibrinogen [-5.5% (CI, -7.8 to -3.2%)] and plasminogen activator inhibitor-1 [-25.1% (CI, -33.6 to -15.5%)]. Oral agents produced larger beneficial effects than transdermal agents, but increased C-reactive protein (CRP) [37.6% (CI, 17.4-61.3%)] and decreased protein S [-8.6% CI, -13.1 to -4.1%)], while transdermal agents had no effect. HRT reduces abdominal obesity, insulin resistance, new-onset diabetes, lipids, blood pressure, adhesion molecules and procoagulant factors in women without diabetes and reduced insulin resistance and fasting glucose in women with diabetes. Oral agents adversely affected CRP and protein S, while transdermal agents had no effects.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Obes Metab Syndr
                Journal ID (iso-abbrev): J Obes Metab Syndr
                Title: Journal of Obesity & Metabolic Syndrome
                Publisher: Korean Society for the Study of Obesity
                ISSN (Print): 2508-6235
                ISSN (Electronic): 2508-7576
                Publication date (Print): September 2017
                Publication date (Electronic): 30 September 2017
                Volume: 26
                Issue: 3
                Pages: 172-180
                Affiliations
                Diabetes Obesity & Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York, USA
                Author notes
                [* ]Corresponding author: Mi-Jeong Lee, http://orcid.org/0000-0002-8171-7913, Diabetes Obesity & Metabolism Institute, Icahn School of Medicine at Mount Sinai, 1 Gustave Levy Place, Box 1152, New York, NY 10029, USA, Tel: +1-212-241-7315, Fax: +1-212-241-7315, E-mail: mi-jeong.lee1@ 123456mssm.edu
                Article
                Publisher ID: jomes-26-172
                DOI: 10.7570/jomes.2017.26.3.172
                PMC ID: 6484911
                PubMed ID: 31089514
                SO-VID: c224a3eb-e646-4da7-bfce-8a5b81c8abce
                Copyright © Copyright © 2017 Korean Society for the Study of Obesity
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 21 July 2017
                Date revision received : 20 August 2017
                Date accepted : 28 August 2017
                Categories
                Subject: Review

                Keywords: estrogen,androgen,fat distribution,adipocyte biology
                Data availability:
                Keywords: estrogen, androgen, fat distribution, adipocyte biology

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