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      Sex differences in metabolic homeostasis, diabetes, and obesity

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      Publication date (Electronic):
      Journal: Biology of Sex Differences
      Publisher: BioMed Central

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          Abstract

          There are fundamental aspects of the control of metabolic homeostasis that are regulated differently in males and females. This sex asymmetry represents an evolutionary paradigm for females to resist the loss of energy stores. This perspective discusses the most fundamental sex differences in metabolic homeostasis, diabetes, and obesity. Together, the role of genetic sex, the programming effect of testosterone in the prenatal period in males, and the activational role of sex hormones at puberty produce two different biological systems in males and females that need to be studied separately. These sex-specific differences in energy homeostasis and metabolic dysfunction represent an untested source of factors that can be harnessed to develop relevant sex-based therapeutic avenues for diabetes, metabolic syndrome, and obesity.

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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.
          Article 0 comments Cited 269 times – based on 0 reviews     Review now
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            Increasing prevalence of the metabolic syndrome among u.s. Adults.

            Earl S. Ford, Wayne Giles, Ali Mokdad (2004)
            The prevalence of the metabolic syndrome is high among U.S. adults. Our purpose was to determine whether the prevalence of this syndrome has changed since 1988-1994. A total of 6,436 men and women aged > or = 20 years from the National Health and Nutrition Examination Survey (NHANES) III (1988-1994) and 1,677 participants from NHANES 1999-2000 were included in the analyses. We used the definition of the metabolic syndrome developed by the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The unadjusted prevalence of the metabolic syndrome was 23.1% in NHANES III and 26.7% in NHANES 1999-2000 (P = 0.043), and the age-adjusted prevalences were 24.1 and 27.0% (P = 0.088), respectively. The age-adjusted prevalence increased by 23.5% among women (P = 0.021) and 2.2% among men (P = 0.831). Increases in high blood pressure, waist circumference, and hypertriglyceridemia accounted for much of the increase in the prevalence of the metabolic syndrome, particularly among women. The increased prevalence of the metabolic syndrome is likely to lead to future increases in diabetes and cardiovascular disease. Copyright 2004 American Diabetes Association
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              Androgens decrease plasma adiponectin, an insulin-sensitizing adipocyte-derived protein.

              Norikazu Maeda, Ken Kishida, H Nagaretani … (2002)
              Adiponectin, an adipose-specific secretory protein, exhibits antidiabetic and antiatherogenic properties. In the present study, we examined the effects of sex hormones on the regulation of adiponectin production. Plasma adiponectin concentrations were significantly lower in 442 men (age, 52.6 +/- 11.9 years [mean +/- SD]) than in 137 women (53.2 +/- 12.0 years) but not different between pre- and postmenopausal women. In mice, ovariectomy did not alter plasma adiponectin levels. In contrast, high levels of plasma adiponectin were found in castrated mice. Testosterone treatment reduced plasma adiponectin concentration in both sham-operated and castrated mice. In 3T3-L1 adipocytes, testosterone reduced adiponectin secretion into the culture media, using pulse-chase study. Castration-induced increase in plasma adiponectin was associated with a significant improvement of insulin sensitivity. Our results indicate that androgens decrease plasma adiponectin and that androgen-induced hypoadiponectinemia may be related to the high risks of insulin resistance and atherosclerosis in men.
              Article 0 comments Cited 153 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Franck Mauvais-Jarvis: 504-988-5990 , fmauvais@tulane.edu
                Journal
                Journal ID (nlm-ta): Biol Sex Differ
                Journal ID (iso-abbrev): Biol Sex Differ
                Title: Biology of Sex Differences
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2042-6410
                Publication date (Electronic): 3 September 2015
                Publication date PMC-release: 3 September 2015
                Publication date Collection: 2015
                Volume: 6
                Electronic Location Identifier: 14
                Affiliations
                Section of Endocrinology & Metabolism, Department of Medicine, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, LA 70112 USA
                Article
                Publisher ID: 33
                DOI: 10.1186/s13293-015-0033-y
                PMC ID: 4559072
                PubMed ID: 26339468
                SO-VID: 62525995-0204-4a9d-b5a6-bd81267315fa
                Copyright © © Mauvais-Jarvis. 2015
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 14 May 2015
                Date accepted : 30 July 2015
                Categories
                Subject: Review
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                issue-copyright-statement © The Author(s) 2015

                ScienceOpen disciplines: Human biology
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                ScienceOpen disciplines: Human biology

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