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      Metabolic syndrome: pathophysiology, management, and modulation by natural compounds

      1 , 2 , 3 , 3
      Therapeutic Advances in Cardiovascular Disease
      SAGE Publications

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          Abstract

          <p class="first" id="d13874364e130">Metabolic syndrome (MetS) represents a cluster of metabolic abnormalities that include hypertension, central obesity, insulin resistance, and atherogenic dyslipidemia, and is strongly associated with an increased risk for developing diabetes and atherosclerotic and nonatherosclerotic cardiovascular disease (CVD). The pathogenesis of MetS involves both genetic and acquired factors that contribute to the final pathway of inflammation that leads to CVD. MetS has gained significant importance recently due to the exponential increase in obesity worldwide. Early diagnosis is important in order to employ lifestyle and risk factor modification. Here, we review the epidemiology and pathogenesis of MetS, the role of inflammation in MetS, and summarize existing natural therapies for MetS. </p>

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          Most cited references32

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          Prevalence of the Metabolic Syndrome Among US Adults

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            Plasma adiponectin levels and risk of myocardial infarction in men.

            Adiponectin, a recently discovered adipocyte-derived peptide, is involved in the regulation of insulin sensitivity and lipid oxidation and, purportedly, in the development of atherosclerosis and coronary heart disease in humans. To assess prospectively whether plasma adiponectin concentrations are associated with risk of myocardial infarction (MI). Nested case-control study among 18 225 male participants of the Health Professionals Follow-up Study aged 40 to 75 years who were free of diagnosed cardiovascular disease at the time of blood draw (1993-1995). During 6 years of follow-up through January 31, 2000, 266 men subsequently developed nonfatal MI or fatal coronary heart disease. Using risk set sampling, controls were selected in a 2:1 ratio matched for age, date of blood draw, and smoking status (n = 532). Incidence of nonfatal MI and fatal coronary heart disease by adiponectin level. After adjustment for matched variables, participants in the highest compared with the lowest quintile of adiponectin levels had a significantly decreased risk of MI (relative risk [RR], 0.39; 95% confidence interval [CI], 0.23-0.64; P for trend <.001). Additional adjustment for family history of MI, body mass index, alcohol consumption, physical activity, and history of diabetes and hypertension did not substantively affect this relationship (RR, 0.41; 95% CI, 0.24-0.70; P for trend <.001). Further adjustment for hemoglobin A1c or C-reactive protein levels also had little impact, but additional adjustment for low- and high-density lipoprotein cholesterol levels modestly attenuated this association (RR, 0.56; 95% CI, 0.32-0.99; P for trend =.02). High plasma adiponectin concentrations are associated with lower risk of MI in men. This relationship can be only partly explained by differences in blood lipids and is independent of inflammation and glycemic status.
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              The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity.

              The metabolic effects of obesity have made this highly prevalent disease one of the most common risk factors for diabetes, hypertension, and atherosclerosis, the leading causes of end-stage renal failure. However, obesity per se, as defined by body mass index, is less predictive of the development of these diseases than is the presence of a constellation of obesity-related abnormalities now known as the metabolic syndrome. Recognition of this syndrome, which can readily be identified in clinical settings using defined threshold values for waist circumference, BP, fasting glucose, and dyslipidemia, allows for earlier intervention in these high-risk patients. Systemic insulin resistance has been implicated as one possible factor that links visceral obesity to adverse metabolic consequences; however, the mechanism whereby adipose tissue causes alterations in insulin sensitivity remains unclear. Infection and inflammation are commonly associated with insulin resistance, and visceral obesity is associated with a chronic, low-grade inflammatory state, suggesting that inflammation may be a potential mechanism whereby obesity leads to insulin resistance. Moreover, adipose tissue is now recognized as an immune organ that secretes numerous immunomodulatory factors and seems to be a significant source of inflammatory signals known to cause insulin resistance. Therefore, inflammation within white adipose tissue may be a crucial step contributing to the emergence of many of the pathologic features that characterize the metabolic syndrome and result in diabetes and atherosclerosis. This review describes the role of proinflammatory cytokines and hormones released by adipose tissue in generating the chronic inflammatory profile associated with visceral obesity.
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                Author and article information

                Journal
                Therapeutic Advances in Cardiovascular Disease
                Therapeutic Advances in Cardiovascular Disease
                SAGE Publications
                1753-9447
                1753-9455
                June 07 2017
                August 2017
                June 22 2017
                August 2017
                : 11
                : 8
                : 215-225
                Affiliations
                [1 ]Division of Cardiovascular Medicine, Westchester Medical Center, Valhalla, NY, USA
                [2 ]Division of Cardiovascular Medicine, Central Arkansas Veterans Healthcare System and University of Arkansas for Medical Sciences, 4301 W. Markham St. #532, Little Rock, AR 72205, USA
                [3 ]Division of Cardiovascular Medicine, Central Arkansas Veterans Healthcare System and University of Arkansas for Medical Sciences, Little Rock, AR, USA
                Article
                10.1177/1753944717711379
                5933580
                28639538
                d714bddd-37da-4134-baa4-b4bddf4ae57b
                © 2017

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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