Metabolic syndrome: what changed during last 30 years?
DOI:
https://doi.org/10.18370/2309-4117.2018.43.15-27Keywords:
metabolic syndrome, obesity, diagnostic criteria, adiposopathy, insulin resistance, obesity with normal weight, metabolically healthy obesity, developmental programming, epigenetics, environmental obesogenes, sympathetic nervous system, hyperandrogenemia,Abstract
Metabolic syndrome (MS) is a cluster of cardiometabolic factors that are strongly associated with the risk of serious chronic diseases. The prevalence of MS continues to grow, including among children, adolescents and people of active reproductive age. For the sphere of reproductive medicine, the problem of MS is of particular importance not only because of its negative impact on fertility, the frequency of complications of pregnancy and childbirth, but also because of its transgenerative effect on the health of offspring: it is proved that each of the components of the metabolic syndrome is a powerful epigenetic factor.
Recent studies have revealed many new facets of the pathogenesis of MS and expanded the range of its etiologic factors beyond the alimentary factors, which determines the possibility of finding new approaches to prevention and treatment of this pathology. The review presents: evolution of diagnostic criteria for MS and reflection of this process in epidemiology and clinical approaches to the disease; epidemiological data on the prevalence of MS in young adults.
A brief overview of a large array of scientific research of the last decade on etiology and pathogenesis of MS, in particular the role of adipose tissue dysfunction of visceral, ileofemoral and ectopic depots, causes of the tendency to prevail in one or another adipose tissue depot, new obesity classification, as well as the role of perinatal and epigenetic, ecological (environmental obesogenes, artificial light contamination), composition of intestinal microbiota, state of the sympathetic nervous system, nutritional deficiencies in the development of obesity and MS is provided. The gender differences of pathogenesis and clinical features of MS, as well as the association of MS with dyshormonal and other pathologies (PCOS, hyperprolactinemia, uterine myoma, endometriosis) of female reproductive health are considered.
References
- O’Neill, S., O’Driscoll, L. “Metabolic syndrome: a closer look at the growing epidemic and its associated pathologies.” Obesity reviews 16.1 (2015): 1–12.
- Smith, C.J., Ryckman, K.K. “Epigenetic and developmental influences on the risk of obesity, diabetes, and metabolic syndrome.” Diabetes, metabolic syndrome and obesity: targets and therapy 8 (2015): 295.
- Oda, Eiji. “Metabolic syndrome: its history, mechanisms, and limitations.” Acta diabetologica 49.2 (2012): 89–95.
- Reaven, G.M. “Role of insulin resistance in human disease.” Diabetes 37 (1988): 1595–1607.
- World Health Organization. Report of a WHO consultation: definition of metabolic syndrome in definition, diagnosis and classification of diabetes mellitus and its complications. Part I: Diagnosis and classification of diabetes mellitus. WHO. Geneva (1999).
- Balkau, B., Charles, M.A. “The European Group for the Study of Insulin Resistance (EGIR): Comment on the provisional report from the WHO consultation.” Diabet Med 16 (1999): 442–3.
- Alberti, K., Mayer, G.M., Zimmet, P., Shaw, J. “Metabolic syndrome – a new world‐wide definition. A consensus statement from the international diabetes federation.” Diabetic medicine 23.5 (2006): 469–80.
- National Cholesterol Education Program (NCEP). “Executive summary of the third report of the NCEP expert panel on detection, evaluation, and treatement of high blood cholesterol in adults (Adult Treatement Panel III).” JAMA 285 (2001): 2486–97.
- Alberti, K.G.M.M., et al. “Harmonizing the metabolic syndrome: a joint interim statement of the international diabetes federation task force on epidemiology and prevention; national heart, lung, and blood institute; American heart association; world heart federation; international atherosclerosis society; and international association for the study of obesity.” Circulation 120.16 (2009): 1640–5.
- Alexander, M., Landsman, P.B., Teutsch, S.M., Haffner, S.M. “NCEP-defined metabolic syndrome, diabetes, andprevalence of coronary heart disease among NHANES III participants age 50 years and older.” Diabetes 52.5 (2003): 1210–4.
- Ritchie, S.A., Connell, J.M. “The link between abdominal obesity, metabolic syndrome and cardiovascular disease.” Nutr Metab Cardiovasc Dis 17.4 (2007): 319–26.
- Desroches, S., Lamarche, B. “The evolving definitions and increasing prevalence of the metabolic syndrome.” Appl Physiol Nutr Metab 32.1 (2007): 23–32.
- Ford, E.S., Giles, W.H., Dietz, W.H. “Prevalence of the Metabolic syndrome among US Adults. Findings from the Third National Health and Nutrition Examination Survey.” JAMA 287 (2002): 356¬9.
- Moore, J.X., et al. “Peer Reviewed: Metabolic Syndrome Prevalence by Race/Ethnicity and Sex in the United States, National Health and Nutrition Examination Survey, 1988–2012.” Preventing chronic disease 14 (2017).
- Nolan, P.B., et al. “Prevalence of metabolic syndrome and metabolic syndrome components in young adults: A pooled analysis.” Preventive medicine reports 7 (2017): 211–5.
- Reddon, H., et al. “Revisiting the evolutionary origins of obesity: lazy versus peppy‐thrifty genotype hypothesis.” Obesity Reviews (2018).
- World Health Organization. “Obesity: preventing and managing the global epidemic. Report of a WHO consultation.” World Health Organ Tech Rep Ser 894 (2000): I-XII, 1–253.
- Wajchenberg, B.L. “Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome.” Endocr Rev 21 (2000): 697–738.
- Poirier, P. “Adiposity and cardiovascular disease: are we using the right definition of obesity?” Eur Heart J 28 (2007): 2047–8.
- Karelis, A.D., St-Pierre, D.H., Conus, F., et al. “Metabolic and body composition factors in subgroupsof obesity: what do we know?” J Clin Endocrinol Metab 89 (2004): 2569–75.
- Reitman, M.L., Arioglu, E., Gavrilova, O., Taylor, S.I. “Lipoatrophy revisited.” Trends Endocrinol Metab 11 (2000): 410–6.
- De Lorenzo, A., et al. “New obesity classification criteria as a tool for bariatric surgery indication.” World journal of gastroenterology 22.2 (2016): 681.
- Snitker, S. “Use of body fatness cutoff points.” Mayo Clin Proc 85 (2010): 1057–8.
- De Lorenzo, A., Deurenberg, P., Pietrantuono, M., et al. “How fat is obese?” Acta Diabetol 40 Suppl 1 (2003): S254–S257.
- Després, J.P., Lemieux, S., Lamarche, B., et al. “The insulin resistance-dyslipidemic syndrome: contribution of visceral obesity and therapeutic implications.” Int J Obes Relat Metab Disord 19 Suppl 1 (1995): S76–S86.
- Banerji, M.A., Chaiken, R.L., Gordon, D., et al. “Does intra-abdominal adipose tissue in black men determine whether NIDDM is insulin-resistant or insulin-sensitive?” Diabetes 44 (1995): 141–6.
- Albu, J.B., Kovera, A.J., Johnson, J.A. “Fat distribution and health in obesity.” Ann N Y Acad Sci 904 (2000): 491–501.
- Grundy, S.M., Adams-Huet, B., Vega, G.L. “Variable contributions of fat content and distribution to metabolic syndrome risk factors.” Metab Syndr Relat Disord 6 (2008): 281–8.
- De Lorenzo, A., Del Gobbo, V., Premrov, M.G., et al. “Normal-weight obese syndrome: early inflammation?” Am J Clin Nutr 85 (2007): 40–5.
- Kosmala, W., Jedrzejuk, D., Derzhko, R., et al. “Left ventricular function impairment in patients with normal-weight obesity: contribution of abdominal fat deposition, profibrotic state, reduced insulin sensitivity, and proinflammatory activation.” Circ Cardiovasc Imaging 5 (2012): 349–56.
- Marques-Vidal, P., Pécoud, A., Hayoz, D., et al. “Normal weight obesity: relationship with lipids, glycaemic status, liver enzymes and inflammation.” Nutr Metab Cardiovasc Dis 20 (2010): 669–75.
- Di Renzo, L., Del Gobbo, V., Bigioni, M., et al. “Body composition analyses in normal weight obese women.” Eur Rev Med Pharmacol Sci 10 (2006): 191–6.
- Marques-Vidal, P., Pécoud, A., Hayoz, D., et al. “Prevalence of normal weight obesity in Switzerland: effect of various definitions.” Eur J Nutr 47 (2008): 251–7.
- Marques-Vidal, P., Chiolero, A., Paccaud, F. “Large differences in the prevalence of normal weight obesity using various cut-offs for excess body fat.” E Spen Eur E J Clin Nutr Metab 3 (2008): e159–e162.
- De Lorenzo, A., Martinoli, R., Vaia, F., Di Renzo, L. “Normal weight obese (NWO) women: an evaluation of a candidate new syndrome.” Nutr Metab Cardiovasc Dis 16 (2006): 513–23.
- Romero-Corral, A., Somers, V.K., Sierra-Johnson, J., et al. “Normal weight obesity: a risk factor for cardiometabolic dysregulation and cardiovascular mortality.” Eur Heart J 31 (2010): 737–46.
- Jean, N., Somers, V.K., Sochor, O., et al. “Normal-weight obesity: implications for cardiovascular health.” Curr Atheroscler Rep 16 (2014): 464.
- Di Renzo, L., Bertoli, A., Bigioni, M., et al. “Body composition and -174G/C interleukin-6 promoter gene polymorphism: association with progression of insulin resistance in normal weight obese syndrome.” Curr Pharm Des 14 (2008): 2699–706.
- Di Renzo, L., Bigioni, M., Bottini, F.G., et al. “Normal Weight Obese syndrome: role of single nucleotide polymorphism of IL-1 5Ralpha and MTHFR 677C--& gt; T genes in the relationship between body composition and resting metabolic rate.” Eur Rev Med Pharmacol Sci 10 (2006): 235–45.
- Di Renzo, L., Gloria-Bottini, F., Saccucci, P., et al. “Role of interleukin-15 receptor alpha polymorphisms in normal weight obese syndrome.” Int J Immunopathol Pharmacol 22 (2009): 105–13.
- Di Renzo, L., Sarlo, F., Petramala, L., et al. “Association between -308 G/A TNF-α polymorphism and appendicular skeletal muscle mass index as a marker of sarcopenia in normal weight obese syndrome.” Dis Markers 35 (2013): 615–23.
- Di Renzo, L., Bigioni, M., Del Gobbo, V., et al. “Interleukin-1 (IL-1) receptor antagonist gene polymorphism in normal weight obese syndrome: relationship to body composition and IL-1 alpha and beta plasma levels.” Pharmacol Res 55 (2007): 131–8.
- Ruderman, N.B., Schneider, S.H., Berchtold, P. “The “metabolically obese”, normal-weight individual.” Am J Clin Nutr 34 (1981): 1617–21.
- Ruderman, N., Chisholm, D., Pi-Sunyer, X., Schneider, S. “The metabolically obese, normal-weight individual revisited. Diabetes 47 (1998): 699–713.
- Dvorak, R.V., DeNino, W.F., Ades, P.A., Poehlman, E.T. “Phenotypic characteristics associated with insulin resistance in metabolically obese but normal-weight young women.” Diabetes 48 (1999): 2210–4.
- Conus, F., Allison, D.B., Rabasa-Lhoret, R., et al. “Metabolic and behavioral characteristics of metabolically obese but normal-weight women.” J Clin Endocrinol Metab 89 (2004): 5013–20.
- Meigs, J.B., Wilson, P.W., Fox, C.S., et al. “Body mass index, metabolic syndrome, and risk of type 2 diabetes or cardiovascular disease.” J Clin Endocrinol Metab 91 (2006): 2906–12.
- Succurro, E., Marini, M.A., Frontoni, S., et al. “Insulin secretion in metabolically obese, but normal weight, and in metabolically healthy but obese individuals.” Obesity (Silver Spring) 16 (2008): 1881–6.
- Eckel, N., Mühlenbruch, K., Meidtner, K., et al. “Characterization of metabolically unhealthy normalweight individuals: Risk factors and their associations with type 2 diabetes.” Metabolism 64 (2015): 862–71.
- Thomas, E.L., Frost, G., Taylor-Robinson, S.D., Bell, J.D. “Excess body fat in obese and normal-weight subjects.” Nutr Res Rev 25 (2012): 150–61.
- Wildman, R.P., Muntner, P., Reynolds, K., et al. “The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering: prevalence and correlates of 2 phenotypes among the US population (NHANES 1999–2004).” Arch Intern Med 168 (2008): 1617–24.
- Yoo, H.K., Choi, E.Y., Park, E.W., et al. “Comparison of Metabolic Characteristics of Metabolically Healthy but Obese (MHO) Middle-Aged Men According to Different Criteria.” Korean J Fam Med 34 (2013): 19–26.
- Singh-Manoux, A., Czernichow, S., Elbaz, A., et al. “Obesity phenotypes in midlife and cognition in early old age: the Whitehall II cohort study.” Neurology 79 (2012): 755–62.
- Calori, G., Lattuada, G., Piemonti, L., et al. “Prevalence, metabolic features, and prognosis of metabolically healthy obese Italian individuals: the Cremona Study.” Diabetes Care 34 (2011): 210–15.
- Lopez-Garcia, E., Guallar-Castillon, P., Leon-Muñoz, L., Rodriguez-Artalejo, F. “Prevalence and determinants of metabolically healthy obesity in Spain.” Atherosclerosis 231 (2013): 152–7.
- Hamer, M., Stamatakis, E. “Metabolically healthy obesity and risk of all-cause and cardiovascular disease mortality.” J Clin Endocrinol Metab 97 (2012): 2482–8.
- Brochu, M., Tchernof, A., Dionne, I.J., et al. “What are the physical characteristics associated with a normal metabolic profile despite a high level of obesity in postmenopausal women?” J Clin Endocrinol Metab 86 (2001): 1020–5.
- Durward, C.M., Hartman, T.J., Nickols-Richardson, S.M. “All-cause mortality risk of metabolically healthy obese individuals in NHANES III.” J Obes (2012): 460321.
- Shea, J.L., Randell, E.W., Sun, G. “The prevalence of metabolically healthy obese subjects defined by BMI and dual-energy X-ray absorptiometry.” Obesity (Silver Spring) 19 (2011): 624–30.
- Manu, P., Ionescu-Tirgoviste, C., Tsang, J., et al. “Dysmetabolic signals in “metabolically healthy”obesity.” Obes Res Clin Pract 6 (2012): e1–e90.
- Arnlöv, J., Ingelsson, E., Sundström, J., Lind, L. “Impact of body mass index and the metabolic syndrome on the risk of cardiovascular disease and death in middle-aged men.” Circulation 121 (2010): 230–6.
- Flint, A.J., Hu, F.B., Glynn, R.J., et al. “Excess weight and the risk of incident coronary heart disease among men and women.” Obesity (Silver Spring) 18 (2010): 377–83.
- Chang, Y., Kim, B.K., Yun, K.E., et al. “Metabolically-healthy obesity and coronary artery calcification.” J Am Coll Cardiol 63 (2014): 2679–86.
- Eshtiaghi, R., Keihani, S., Hosseinpanah, F., et al. “Natural course of metabolically healthy abdominal obese adults after 10 years of follow-up: the Tehran Lipid and Glucose Study.” Int J Obes (Lond) 39 (2015): 514–9.
- Kramer, C.K., Zinman, B., Retnakaran, R. “Are metabolically healthy overweight and obesity benign conditions? A systematic review and meta-analysis.” Ann Intern Med 159 (2013): 758–69.
- Després, J.P. “Body fat distribution and risk of cardiovascular disease: an update.” Circulation 126 (2012): 1301–13.
- Bays, H., Abate, N., Chandalia, M. “Adiposopathy: sick fat causes high blood sugar, high blood pressure and dyslipidemia.” Future Cardiol 1 (2005): 39–59.
- Bays, H., Ballantyne, C. “Adiposopathy: why do adiposity and obesity cause metabolic disease?” Future Lipidol 1 (2006): 389–420.
- Bays, H. “Adiposopathy, “sick fat,” Ockham’s razor, and resolution of the obesity paradox.” Curr Atheroscler Rep 16 (2014): 409.
- Smith, S.R., et al. “Contributions of total body fat, abdominal subcutaneous adipose tissue compartments, and visceral adipose tissue to the metabolic complications of obesity.” Metabolism-Clinical and Experimental 50.4 (2001): 425–35.
- Ross, R., Leger, L., Morris, D., et al. “Quantification of adipose tissue by MRI: relationship with anthropometric variables.” J Appl Physiol 72 (1992): 787–95.
- Frayn, K.N. “Adipose tissue as a buffer for daily lipid flux.” Diabetologia 45 (2002): 1201–10.
- Knittle, J.L., Timmers, K., Ginsberg-Fellner, F., et al. “The growth of adipose tissue in children and adolescents. Cross-sectional and longitudinal studies of adipose cell number and size.” J Clin Invest 63 (1979): 239–46.
- Spalding, K.L., Arner, E., Westermark, P.O., et al. “Dynamics of fat cell turnover in humans.” Nature 453 (2008): 783–7.
- Lee, M.J., Wu, Y., Fried, S.K. “Adipose tissue heterogeneity: implication of depot differences in adipose tissue for obesity complications.” Mol Aspects Med 34 (2013): 1–11.
- Karastergiou, K., Smith, S.R., Greenberg, A.S., Fried, S.K. “Sex differences in human adipose tissues – the biology of pear shape.” Biol Sex Differ 3 (2012): 13.
- Tchernof, A., Després, J.-P. “Pathophysiology of human visceral obesity: an update.” Physiological reviews 93.1 (2013): 359–404.
- Lafontan, M. “Adipose tissue and adipocyte dysregulation.” Diabetes & Metabolism 40.1 (2014): 16–28.
- Goossens, G.H. “The metabolic phenotype in obesity: fat mass, body fat distribution, and adipose tissue function.” Obesity facts 10.3 (2017): 207–15.
- Yang, X., Smith, U. “Adipose tissue distribution and risk of metabolic disease: does thiazolidinedione-induced adipose tissue redistribution provide a clue to the answer?” Diabetologia 50.6 (2007): 1127–39.
- Fried, S.K., Mi‐Jeong, L., Karastergiou. K. “Shaping fat distribution: New insights into the molecular determinants of depot‐and sex‐dependent adipose biology.” Obesity 23.7 (2015): 1345–52.
- Morgan-Bathke, M., Chen, L., Oberschneider, E., et al. “Sex and depot differences in ex vivo adipose tissue fatty acid storage and glycerol-3-phosphate acyltransferase activity.” Am J Physiol Endocrinol Metab (2015).
- Baumann, H., Gauldie, J. “Regulation of hepatic acute phase plasma protein genes by hepatocyte stimulating factors and other mediators of inflammation.” Mol Biol Med 7 (1990): 147–59.
- Fernandez-Real, J.M., Vayreda, M., Richart, C., et al. “Circulating interleukin 6 levels, blood pressure, and insulin sensitivity in apparently healthy men and women.” J Clin Endocrinol Metab 86 (2001): 1154–9.
- Sopasakis, V.R., Sandqvist, M., Gustafson, B., et al. “High local concentrations and effects on differentiation implicate interleukin-6 as a paracrine regulator.” Obes Res 12 (2004): 454–60.
- Dusserre, E., Moulin, P., Vidal, H. “Differences in mRNA expression of the proteins secreted by the adipocytes in human subcutaneous and visceral adipose tissues.” Biochim Biophys Acta 1500 (2000): 88–96.
- Van Harmelen, V., Rohrig, K., Hauner, H. “Comparison of proliferation and differentiation capacity of human adipocyte precursor cells from the omental and subcutaneous adipose tissue depot of obese subjects.” Metabolism 53 (2004): 632–7.
- Frayn, K.N. “Adipose tissue as a buffer for daily lipid flux.” Diabetologia 45 (2002): 1201–10.
- Ravussin, E., Smith, S.R. “Increased fat intake, impaired fat oxidation, and failure of fat cell proliferation result in ectopic fat storage, insulin resistance, and type 2 diabetes mellitus.” Ann N Y Acad Sci 967 (2002): 363–78.
- Tritos, N.A., Mantzoros, C.S. “Leptin: its role in obesity and beyond.” Diabetologia 40 (1997): 1371–9.
- Montague, C.T., Prins, J.B., Sanders, L., et al. “Depot- and sex-specific differences in human leptin mRNA expression: implications for the control of regional fat distribution.” Diabetes 46 (1997): 342–7.
- Hamilton, B.S., Paglia, D., Kwan, A.Y., Deitel, M. “Increased obese mRNA expression in omental fat cells from massively obese humans.” Nat Med 1 (1995): 953–6.
- Wells, J.C. “Sexual dimorphism of body composition.” Best Pract Res Clin Endocrinol Metab 21 (2007): 415–30.
- Horber, F.F., Zurcher, R.M., Herren, H., et al. “Altered body fat distribution in patients with glucocorticoid treatment and in patients on long-term dialysis.” Am J Clin Nutr 43 (1986): 758–69.
- Malis, C., Rasmussen, E.L., Poulsen, P., et al. “Total and regional fat distribution is strongly influenced by genetic factors in young and elderly twins.” Obes Res 13 (2005): 2139–45.
- Hilton, C., Karpe, F., Pinnick, K.E. “Role of developmental transcription factors in white, brown and beige adipose tissues.” Biochim Biophys Acta 1851 (2015): 686–96.
- Pinnick, K.E., Nicholson, G., Manolopoulos, K.N., et al. “Distinct developmental profile of lower-body adipose tissue defines resistance against obesity-associated metabolic complications.” Diabetes 63 (2014): 3785–97.
- Shungin, D., Winkler, T.W., Croteau-Chonka, D.C., et al. “New genetic loci link adipose and insulin biology to body fat distribution.” Nature 518 (2015): 187–96.
- Heid, I.M., Jackson, A.U., Randall, J.C., et al. “Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution.” Nat Genet 42 (2010): 949–60.
- Ehrmann, D.A., et al. “Prevalence and predictors of the metabolic syndrome in women with polycystic ovary syndrome.” The Journal of Clinical Endocrinology & Metabolism 91.1 (2006): 48–53. 10.1210/jc.2005-1329
- Couto, A.A., et al. “Metabolic profiling of polycystic ovary syndrome reveals interactions with abdominal obesity.” International Journal of Obesity 41.9 (2017): 1331.
- Thorne, A., Lonnqvist, F., Apelman, J., et al. “A pilot study of long-term effects of a novel obesity treatment: omentectomy in connection with adjustable gastric banding.” Int J Obes Relat Metab Disord 26 (2002): 193–9.
- Giese, S.Y., Bulan, E.J., Commons, G.W., et al. “Improvements in cardiovascular risk profile with largevolume liposuction: a pilot study.” Plast Reconstr Surg 108 (2001): 510–21.
- Gonzalez-Ortiz, M., Robles-Cervantes, J.A., Cardenas-Camarena, L., et al. “The effects of surgically removing subcutaneous fat on the metabolic profile and insulin sensitivity in obese women after large-volume liposuction treatment.” Horm Metab Res 34 (2002): 446–9.
- Cazes, L., Deitel, M., Levine, R.H. “Effect of abdominal lipectomy on lipid profile, glucose handling and blood pressure in patients with truncal obesity.” Obes Surg 6 (1996): 159–66.
- Klein, S., Fontana, L., Young, V.L., et al. “Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease.” N Engl J Med 350 (2004): 2549–57.
- Matarasso, A., Kim, R.W., Kral, J.G. “The impact of liposuction on body fat.” Plast Reconstr Surg 102 (1998): 1686–9.
- Tobi, E.W., Goeman, J.J., Monajemi, R., et al. “DNA methylation signatures link prenatal famine exposure to growth and metabolism.” Nat Commun 5 (2014): 5592.
- Hales, C.N., Barker, D.J. “Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis.” Diabetologia 35.7 (1992): 595–601.
- Cardozo, E., Pavone, M.E., Hirshfeld-Cytron, J.E. “Metabolic syndrome and oocyte quality.” Trends Endocrinol Metab 22.3 (2011): 103–9.
- Robker, R.L. “Evidence that obesity alters the quality of oocytes and embryos.” Pathophysiology 15.2 (2008): 115–21.
- Gravina, S., Vijg, J. “Epigenetic factors in aging and longevity.” Pflügers Archiv-European Journal of Physiology 459.2 (2010): 247–58.
- Tammen, S.A., Friso, S., et al. “Epigenetics: the link between nature and nurture.” Molecular aspects of medicine 34.4 (2013): 753–64.
- Franklin, T.B., et al. “Epigenetic transmission of the impact of early stress across generations.” Biological psychiatry 68.5 (2010): 408–15.
- Ponzio, B.F., Carvalho, M.H., Fortes, Z.B., do Carmo Franco, M. “Implications of maternal nutrient restriction in transgenerational programming of hypertension and endothelial dysfunction across F1-F3 offspring.” Life Sci 90.15–16 (2012): 571–7.
- Gray, C., Vickers, M.H., Segovia, S.A., et al. “A maternal high fat diet programmes endothelial function and cardiovascular status in adult male offspring independent of body weight, which is reversed by maternal conjugated linoleic acid (CLA) supplementation.” PloS One 10.2 (2015): e0115994.
- Kaar, J.L., Crume, T., Brinton, J.T., et al. “Maternal obesity, gestational weight gain, and offspring adiposity: the exploring perinatal outcomes among children study.” J Pediatr 165.3 (2014): 509–15.
- Briffa, J.F., McAinch, A.J., Romano, T., et al. “Leptin in pregnancy and development: a contributor to adulthood disease?” Am J Physiol Endocrinol Metab 308.5 (2015): E335–E350.
- Fisman, E.Z., Tenenbaum, A. “Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?” Cardiovasc Diabetol 13 (2014):103.
- Fan, L., Lindsley, S.R., Comstock, S.M., et al. “Maternal high-fat diet impacts endothelial function in nonhuman primate offspring.” Int J Obes (Lond) 37.2 (2013): 254–62.
- Doblado, M., Moley, K.H. “Glucose metabolism in pregnancy and embryogenesis.” Curr Opin Endocrinol Diabetes Obes 14.6 (2007): 488–93.
- Brown, R.E., Sharma, A.M., Ardern, C.I., et al. “Secular differences in the association between caloric intake, macronutrient intake, and physical activity with obesity.” Obes Res Clin Pract 10 (2016): 243–55.
- Grun, F., Blumberg, B. “Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling.” Endocrinology 147 (2006): S50–55.
- Heindel, J.J., Blumberg, B., Cave, M., et al. “Metabolism disrupting chemicals and metabolic disorders.” Reprod Toxicol 68 (2017): 3–33.
- Janesick, A., Blumberg, B. “Endocrine disruptting chemicals and the developmental programming of adipogenesis and obesity.” Birth Defects Res C Embryo Today 93 (2011): 34–50.
- Janesick, A.S., Blumberg, B. “Obesogens: an emerging threat to public health.” Am J Obstet Gynecol 214 (2016): 559–65.
- Cappuccio, F.P., et al. “Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis.” Diabetes care 33.2 (2010): 414–20.
- Mugnai, G., Danese, A. “Sleep Deprivation and Metabolic Syndrome.” Modulation of Sleep by Obesity, Diabetes, Age, and Diet (2015): 185–92.
- Zubidat, A.E., Abraham, H. “Artificial light-at-night – a novel lifestyle risk factor for metabolic disorder and cancer morbidity.” Journal of basic and clinical physiology and pharmacology 28.4 (2017): 295–313.
- Dahiya, D.K., et al. “Gut microbiota modulation and its relationship with obesity using prebiotic fibers and probiotics: a review.” Frontiers in microbiology 8 (2017): 563.
- Thorp, A.A., Schlaich, M.P. “Relevance of sympathetic nervous system activation in obesity and metabolic syndrome.” Journal of diabetes research 2015 (2015).
- Jarhult, J., Falck, B., Ingemansson, S., Nobin, A. “The functional importance of sympathetic nerves to the liver and endocrine pancreas.” Annals of Surgery 189.1 (1979): 96–100.
- Masuo, K., Mikami, H., Ogihara, T., Tuck, M.L. “Sympathetic nerve hyperactivity precedes hyperinsulinemia and blood pressure elevation in a young, nonobese Japanese population.” American Journal of Hypertension 10.1 (1997): 77–83.
- Flaa, A., Aksnes, T.A., Kjeldsen, S.E., et al. “Increased sympathetic reactivity may predict insulin resistance: an 18-year follow-up study.” Metabolism: Clinical and Experimental 57.10 (2008): 1422–7.
- Carnethon, M.R., Golden, S.H., Folsom, A.R., et al. “Prospective investigation of autonomic nervous system function and the development of type 2 diabetes: the atherosclerosis risk in communities study, 1987–1998.” Circulation 107.17 (2003): 2190–5.
- Lee, Z.S.K., Critchley, J.A.J.H., Tomlinson, B., et al. “Urinary epinephrine and norepinephrine interrelations with obesity, insulin, and the metabolic syndrome in Hong Kong Chinese.” Metabolism: Clinical and Experimental 50.2 (2001): 135–43.
- Vaz, M., Jennings, G., Turner, A., et al. “Regional sympathetic nervous activity and oxygen consumption in obese normotensive human subjects.” Circulation 96.10 (1997): 3423–9.
- Straznicky, N.E., Lambert, E.A., Lambert, G.W., et al. “Effects of dietary weight loss on sympathetic activity and cardiac risk factors associated with the metabolic syndrome.” Journal of Clinical Endocrinology and Metabolism 90.11 (2005): 5998–6005.
- Straznicky, N.E., Eikelis, N., Lambert, E.A., Esler, M.D. “Mediators of sympathetic activation in metabolic syndrome obesity.” Current Hypertension Reports 10.6 (2008): 440–7.
- Gentile, C.L., Orr, J.S., Davy, B.M., Davy, K.P. “Modest weight gain is associated with sympathetic neural activation in nonobese humans.” The American Journal of Physiology – Regulatory Integrative and Comparative Physiology 292.5 (2007): R1834–R1838.
- Brunner, E.J., Hemingway, H., Walker, B.R., et al. “Adrenocortical, autonomic, and inflammatory causes of the metabolic syndrome: nested case-control study.” Circulation 106.21 (2002): 2659–65.
- Rochlani, Yogita, Naga Venkata Pothineni, and Jawahar L. Mehta. “Metabolic syndrome: does it differ between women and men?» Cardiovascular drugs and therapy 29.4 (2015): 329–38.
- Teede, H.J., et al. “Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome.” Fertility and Sterility (2018).
- NIH: Office of Disease Prevention. Polycystic Ovary Syndrome, Pathways to Prevention (2012). Available from: [https://prevention-archive.od.nih.gov/docs/programs/pcos/FinalReport.pdf].
- Lim, S.S., et al. “Metabolic syndrome in polycystic ovary syndrome: a systematic review, meta‐analysis and meta‐regression.” Obesity Reviews (2018).
- Condorelli, R.A., et al. “Androgen excess and metabolic disorders in women with PCOS: beyond the body mass index.” Journal of endocrinological investigation (2017): 1–6.
- Knudtzon, J., Johansen, P.W., Haug, E., et al. “Effects of hypersecretion of growth hormone and prolactin on plasma levels of glucagon and insulin in GH3-cell-tumor-bearing rats, and the influence of bromocriptine treatment.” Life Sci 39 (1986): 617–21.
- Byatt, J.C., Staten, N.R., Salsgiver, W.J., et al. “Stimulation of food intake and weight gain in mature female rats by bovine prolactin and bovine growth hormone.” Am J Physiol 264 (1993): E986–E992.
- Bole-Feysot, C., Goffin, V., Edery, M., et al. “Prolactin (PRL) and its receptor: actions, signal transduction pathways and phenotypes observed in PRL receptor knockout mice.” Endocr Rev 19 (1998): 225–68.
- Ben-Jonathan, N., Hugo, E.R., Brandebourg, T.D., et al. “Focus on prolactin as a metabolic hormone.” Trends Endocrinol Metab 17 (2006): 110–6.
- Baptista, T., Lacruz, A., De Mendoza, S., et al. “Body weight gain after administration of antipsychotic drugs: correlation with leptin, insulin and reproductive hormones.” Pharmacopsychiatry 33 (2000): 81–8.
- Doknic, M., Pekic, S., Zarkovic, M., et al. “Dopaminergic tone and obesity: an insight from prolactinomas treated with bromocriptine.” Eur J Endocrinol 147 (2002): 77–84.
- Greenman, Y., Tordjman, K., Stern, N. “Increased body weight associated with prolactin secreting pituitary adenomas: weight loss with normalization of prolactin levels.” Clin Endocrinol (Oxf) 48 (1998): 547–53.
- Colao, A., Sarno, A., Cappabianca, P., et al. “Gender differences in the prevalence, clinical features and response to cabergoline in hyperprolactinemia.” Eur J Endocrinol 148.3 (2003): 325–31.
- Augustine, R.A., Grattan, D.R. “Induction of central leptin resistance in hyperphagic pseudopregnant rats by chronic prolactin infusion.” Endocrinology 149 (2008): 1049–55.
- Kok, P., Roelfsema, F., Frolich, M., et al. “Prolactin release is enhanced in proportion to excess visceral fat in obese women.” J Clin Endocrinol Metab 89 (2004): 4445–9.
- Weinhaus, A.J., Stout, L.E., Bhagroo, N.V., et al. “Regulation of glucokinase in pancreatic islets by prolactin: a mechanism for increasing glucose-stimulated insulin secretion during pregnancy.” J Endocrinol 193 (2007): 367–81.
- Brelje, T.C., Stout, L.E., Bhagroo, N.V., et al. “Distinctive roles for prolactin and growth hormone in the activation of signal transducer and activator of transcription 5 in pancreatic islets of Langerhans.” Endocrinology 145 (2004): 4162–75.
- Johnston, D.G., Alberti, K.G., Nattrass, M., et al. “Hyperinsulinaemia in hyperprolactinaemic women.” Clin Endocrinol (Oxf) 13 (1980): 361–8.
- Kong, Shujun, et al. “Association of Hyperglycemia, Hyperlipemia with the Risk of Uterine Leiomyomata: A Case-Control Study.” Cancer Cell Research 2.1 (2014): 37–41.
- Uimari, Outi, et al. “Uterine fibroids and cardiovascular risk.” Human Reproduction 31.12 (2016): 2689–703.
- Haan, Yentl C., et al. “The risk of hypertension and cardiovascular disease in women with uterine fibroids.” The Journal of Clinical Hypertension 20.4 (2018): 718–26.
- Yang, Ying, et al. “Association of body size and body fat distribution with uterine fibroids among Chinese women.” Journal of Women’s Health 23.7 (2014): 619–26.
- Haan, Yentl C., et al. “Hypertension risk in Dutch women with symptomatic uterine fibroids.” American journal of hypertension 28.4 (2014): 487–92.
- Faerstein, E., Szklo, M., Rosenshein, N. “Risk factors for uterine leiomyoma:a practice-based case-control study. I. African-American heritage, reproductive history, body size, and smoking.” Am J Epidemiol 153 (2001): 1.
- Wise, L.A., Palmer, J.R., Spiegelman, D., et al. “Influence of body size and body fat distribution on risk of uterine leiomyomata in U.S. black women.” Epidemiology 16 (2005): 346–5.
- Eckel, R.H., Grundy, S.M., Zimmet, P.Z. “The metabolic syndrome.” Lancet 365 (2005): 1415–28.
- Hebbar, S., Chaya, V., Rai, L., et al. “Factors influencing endometrial thickness in postmenopausal women.” Ann Med Health Sci Res 4 (2014): 608–14.
- Hou, Z.M., Sun, Q., Liu, Y.-Z., et al. “Effects of insulin resistance on myometrial growth.” Int J Clin Exp Med 8 (2015): 1552–7.
- Tak, Young Jin, et al. “Association between uterine leiomyoma and metabolic syndrome in parous premenopausal women: A case-control study.” Medicine 95.46 (2016).
- Kvaskoff, M., et al. “Endometriosis: a high-risk population for major chronic diseases?” Human reproduction update 21.4 (2015): 500–16.
- Soares, M.J., et al. “Vitamin D status and calcium intake in systemic inflammation, insulin resistance and the metabolic syndrome: an update on current evidence.” Trends in Food Science & Technology 62 (2017): 79–90. 10.1016/j.tifs.2017.01.009
- Sarrafzadegan, N., et al. “Magnesium status and the metabolic syndrome: A systematic review and meta-analysis.” Nutrition 32.4 (2016): 409–17.
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