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      Sexual dimorphism of cardiometabolic dysfunction: Gut microbiome in the play?

      review-article
      Author(s): 1 , 2 , 2 , 1 , 2 , ∗
      Publication date (Electronic):
      Journal: Molecular Metabolism
      Publisher: Elsevier
      Keywords: Sex differences, Steroids, Gut microbiota, Metabolic disease, Cardiovascular disease, ApoE, apolipoprotein E, BAs, bile acids, CVD, cardiovascular diseases, E1, estrone, E2, estradiol, E3, estriol, ER, estrogen receptor, FCG, four core genotypes, FMO3, flavin monooxygenases 3, FXR, farnesoid X receptor, GI, gastrointestinal, GPR30, G protein-coupled receptor 30, HDL-c, high-density lipoprotein cholesterol, IBD, inflammatory bowel disease, IBS, irritable bowel syndrome, LDL-c, low-density lipoprotein cholesterol, LPS, lipopolysaccharides, MUC2, mucin-2, NOD, non-obese diabetic, SHP, small heterodimer partner, T1D, type 1 diabetes, T2D, type 2 diabetes, TLR4, Toll-like receptor 4, TMA, trimethylamine, TUDCA, tauroursodeoxycholic acid, ZO-1, zonula occludens

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          Abstract

          Background

          Sex is one of the most powerful modifiers of disease development. Clear sexual dimorphism exists in cardiometabolic health susceptibility, likely due to differences in sex steroid hormones. Changes in the gut microbiome have been linked with the development of obesity, type 2 diabetes, and atherosclerosis; however, the impact of microbes in sex-biased cardiometabolic disorders remains unclear. The gut microbiome is critical for maintaining a normal estrous cycle, testosterone levels, and reproductive function. Gut microbes modulate the enterohepatic recirculation of estrogens and androgens, affecting local and systemic levels of sex steroid hormones. Gut bacteria can also generate androgens from glucocorticoids.

          Scope of review

          This review summarizes current knowledge of the complex interplay between sexual dimorphism in cardiometabolic disease and the gut microbiome.

          Major conclusions

          Emerging evidence suggests the role of gut microbiome as a modifier of disease susceptibility due to sex; however, the impact on cardiometabolic disease in this complex interplay is lacking. Elucidating the role of gut microbiome on sex-biased susceptibility in cardiometabolic disease is of high relevance to public health given its high prevalence and significant financial burden.

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          Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013.

          Marie Ng, Tom Fleming, Margaret W. Robinson … (2015)
          In 2010, overweight and obesity were estimated to cause 3·4 million deaths, 3·9% of years of life lost, and 3·8% of disability-adjusted life-years (DALYs) worldwide. The rise in obesity has led to widespread calls for regular monitoring of changes in overweight and obesity prevalence in all populations. Comparable, up-to-date information about levels and trends is essential to quantify population health effects and to prompt decision makers to prioritise action. We estimate the global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013. We systematically identified surveys, reports, and published studies (n=1769) that included data for height and weight, both through physical measurements and self-reports. We used mixed effects linear regression to correct for bias in self-reports. We obtained data for prevalence of obesity and overweight by age, sex, country, and year (n=19,244) with a spatiotemporal Gaussian process regression model to estimate prevalence with 95% uncertainty intervals (UIs). Worldwide, the proportion of adults with a body-mass index (BMI) of 25 kg/m(2) or greater increased between 1980 and 2013 from 28·8% (95% UI 28·4-29·3) to 36·9% (36·3-37·4) in men, and from 29·8% (29·3-30·2) to 38·0% (37·5-38·5) in women. Prevalence has increased substantially in children and adolescents in developed countries; 23·8% (22·9-24·7) of boys and 22·6% (21·7-23·6) of girls were overweight or obese in 2013. The prevalence of overweight and obesity has also increased in children and adolescents in developing countries, from 8·1% (7·7-8·6) to 12·9% (12·3-13·5) in 2013 for boys and from 8·4% (8·1-8·8) to 13·4% (13·0-13·9) in girls. In adults, estimated prevalence of obesity exceeded 50% in men in Tonga and in women in Kuwait, Kiribati, Federated States of Micronesia, Libya, Qatar, Tonga, and Samoa. Since 2006, the increase in adult obesity in developed countries has slowed down. Because of the established health risks and substantial increases in prevalence, obesity has become a major global health challenge. Not only is obesity increasing, but no national success stories have been reported in the past 33 years. Urgent global action and leadership is needed to help countries to more effectively intervene. Bill & Melinda Gates Foundation. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            Annual medical spending attributable to obesity: payer-and service-specific estimates.

            Eric Finkelstein, Justin G Trogdon, Joel W Cohen … (2009)
            In 1998 the medical costs of obesity were estimated to be as high as $78.5 billion, with roughly half financed by Medicare and Medicaid. This analysis presents updated estimates of the costs of obesity for the United States across payers (Medicare, Medicaid, and private insurers), in separate categories for inpatient, non-inpatient, and prescription drug spending. We found that the increased prevalence of obesity is responsible for almost $40 billion of increased medical spending through 2006, including $7 billion in Medicare prescription drug costs. We estimate that the medical costs of obesity could have risen to $147 billion per year by 2008.
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              Improvement of Insulin Sensitivity after Lean Donor Feces in Metabolic Syndrome Is Driven by Baseline Intestinal Microbiota Composition

              Ruud S Kootte, Evgeni Levin, Jarkko Salojärvi … (2017)
              The intestinal microbiota has been implicated in insulin resistance, although evidence regarding causality in humans is scarce. We therefore studied the effect of lean donor (allogenic) versus own (autologous) fecal microbiota transplantation (FMT) to male recipients with the metabolic syndrome. Whereas we did not observe metabolic changes at 18 weeks after FMT, insulin sensitivity at 6 weeks after allogenic FMT was significantly improved, accompanied by altered microbiota composition. We also observed changes in plasma metabolites such as γ-aminobutyric acid and show that metabolic response upon allogenic FMT (defined as improved insulin sensitivity 6 weeks after FMT) is dependent on decreased fecal microbial diversity at baseline. In conclusion, the beneficial effects of lean donor FMT on glucose metabolism are associated with changes in intestinal microbiota and plasma metabolites and can be predicted based on baseline fecal microbiota composition.
              Article 0 comments Cited 383 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Tzu-Wen L. Cross
                Kazuyuki Kasahara
                Federico E. Rey
                Journal
                Journal ID (nlm-ta): Mol Metab
                Journal ID (iso-abbrev): Mol Metab
                Title: Molecular Metabolism
                Publisher: Elsevier
                ISSN (Electronic): 2212-8778
                Publication date PMC-release: 30 May 2018
                Publication date Collection: September 2018
                Publication date (Electronic): 30 May 2018
                Volume: 15
                Pages: 70-81
                Affiliations
                [1 ]Cardiovascular Research Center, University of Wisconsin-Madison, Madison, WI, 53705, United States
                [2 ]Department of Bacteriology, University of Wisconsin-Madison, Madison, WI, 53706, United States
                Author notes
                [∗ ]Corresponding author. University of Wisconsin-Madison, 5157 Microbial Sciences Building, 1550 Linden Drive, Madison, WI, 53706, United States. ferey@ 123456wisc.edu
                Article
                Publisher ID: S2212-8778(18)30331-4
                DOI: 10.1016/j.molmet.2018.05.016
                PMC ID: 6066746
                PubMed ID: 29887245
                SO-VID: ae94034a-1c25-4f5a-a9b3-148efb581a46
                Copyright © © 2018 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 3 April 2018
                Date revision received : 22 May 2018
                Date accepted : 24 May 2018
                Categories
                Subject: Review

                Keywords: sex differences,steroids,gut microbiota,metabolic disease,cardiovascular disease,apoe, apolipoprotein e,bas, bile acids,cvd, cardiovascular diseases,e1, estrone,e2, estradiol,e3, estriol,er, estrogen receptor,fcg, four core genotypes,fmo3, flavin monooxygenases 3,fxr, farnesoid x receptor,gi, gastrointestinal,gpr30, g protein-coupled receptor 30,hdl-c, high-density lipoprotein cholesterol,ibd, inflammatory bowel disease,ibs, irritable bowel syndrome,ldl-c, low-density lipoprotein cholesterol,lps, lipopolysaccharides,muc2, mucin-2,nod, non-obese diabetic,shp, small heterodimer partner,t1d, type 1 diabetes,t2d, type 2 diabetes,tlr4, toll-like receptor 4,tma, trimethylamine,tudca, tauroursodeoxycholic acid,zo-1, zonula occludens
                Data availability:
                Keywords: sex differences, steroids, gut microbiota, metabolic disease, cardiovascular disease, apoe, apolipoprotein e, bas, bile acids, cvd, cardiovascular diseases, e1, estrone, e2, estradiol, e3, estriol, er, estrogen receptor, fcg, four core genotypes, fmo3, flavin monooxygenases 3, fxr, farnesoid x receptor, gi, gastrointestinal, gpr30, g protein-coupled receptor 30, hdl-c, high-density lipoprotein cholesterol, ibd, inflammatory bowel disease, ibs, irritable bowel syndrome, ldl-c, low-density lipoprotein cholesterol, lps, lipopolysaccharides, muc2, mucin-2, nod, non-obese diabetic, shp, small heterodimer partner, t1d, type 1 diabetes, t2d, type 2 diabetes, tlr4, toll-like receptor 4, tma, trimethylamine, tudca, tauroursodeoxycholic acid, zo-1, zonula occludens

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