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      Prevalence and Correlates of Metabolic Syndrome in the Adolescents of Rural Wardha

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          Abstract

          Background and Objective:

          Metabolic syndrome is a major concern as a precursor of cardiometabolic diseases. The present study was designed to study the magnitude and correlates of metabolic syndrome among the adolescents of rural Wardha.

          Materials and Methods:

          A cross-sectional study was carried out among the adolescents (10-19 years) of Anji PHC. A sample of 405 was selected by random sampling from the sampling frame available with department of Community Medicine. We collected data about their sociodemographic variables and other cardiometabolic risk factors. Fasting blood sample was collected to measure lipid profile and blood glucose. Blood pressure and anthropometric measurements (height, weight, and waist circumference) were also taken.

          Results:

          Prevalence of metabolic syndrome using ATP-III criteria modified for adolescents was found to be 9.9% (95% CI: 7.3-13.1) in the study population and lower level of high-density lipoprotein (HDL) cholesterol was found with a prevalence of 58.3% (95% CI: 53.4-63.0). The prevalence of metabolic syndrome was found to be significantly ( P < 0.05) associated with the presence of obesity and hypertension among family members.

          Interpretation:

          There was a moderately high prevalence of metabolic syndrome among rural adolescents.

          Conclusion:

          The early identification of cardiometabolic risk factors such as hypertension and obesity can help prevent metabolic syndrome, diabetes, and cardiovascular disease.

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          Most cited references21

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Cardiovascular morbidity and mortality associated with the metabolic syndrome.

            To estimate the prevalence of and the cardiovascular risk associated with the metabolic syndrome using the new definition proposed by the World Health Organization A total of 4,483 subjects aged 35-70 years participating in a large family study of type 2 diabetes in Finland and Sweden (the Botnia study) were included in the analysis of cardiovascular risk associated with the metabolic syndrome. In subjects who had type 2 diabetes (n = 1,697), impaired fasting glucose (IFG)/impaired glucose tolerance (IGT) (n = 798) or insulin-resistance with normal glucose tolerance (NGT) (n = 1,988), the metabolic syndrome was defined as presence of at least two of the following risk factors: obesity, hypertension, dyslipidemia, or microalbuminuria. Cardiovascular mortality was assessed in 3,606 subjects with a median follow-up of 6.9 years. In women and men, respectively, the metabolic syndrome was seen in 10 and 15% of subjects with NGT, 42 and 64% of those with IFG/IGT, and 78 and 84% of those with type 2 diabetes. The risk for coronary heart disease and stroke was increased threefold in subjects with the syndrome (P < 0.001). Cardiovascular mortality was markedly increased in subjects with the metabolic syndrome (12.0 vs. 2.2%, P < 0.001). Of the individual components of the metabolic syndrome, microalbuminuria conferred the strongest risk of cardiovascular death (RR 2.80; P = 0.002). The WHO definition of the metabolic syndrome identifies subjects with increased cardiovascular morbidity and mortality and offers a tool for comparison of results from diferent studies.
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              Inflammation: the link between insulin resistance, obesity and diabetes.

              Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory mediators or indices predicts the future development of obesity and diabetes. Two mechanisms might be involved in the pathogenesis of inflammation. Firstly, glucose and macronutrient intake causes oxidative stress and inflammatory changes. Chronic overnutrition (obesity) might thus be a proinflammatory state with oxidative stress. Secondly, the increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. This might interfere with the anti-inflammatory effect of insulin, which in turn might promote inflammation.
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                Author and article information

                Journal
                Indian J Community Med
                Indian J Community Med
                IJCM
                Indian Journal of Community Medicine : Official Publication of Indian Association of Preventive & Social Medicine
                Medknow Publications & Media Pvt Ltd (India )
                0970-0218
                1998-3581
                Jan-Mar 2015
                : 40
                : 1
                : 43-48
                Affiliations
                [1]Department of Biochemistry, Mahatma Gandhi Institute of Medical Sciences, Maharashtra, India
                [1 ]Department of Community Medicine, Mahatma Gandhi Institute of Medical Sciences, Maharashtra, India
                Author notes
                Address for correspondence: Prof. Pradeep R. Deshmukh, Department of Community Medicine, Mahatma Gandhi Institute of Medical Sciences, Sewagram - 442 102, Maharashtra, India. E-mail: prdeshmukh@ 123456gmail.com
                Article
                IJCM-40-43
                10.4103/0970-0218.149270
                4317980
                7889861a-5235-4171-b0a9-141801f0066c
                Copyright: © Indian Journal of Community Medicine

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 January 2013
                : 09 May 2013
                Categories
                Original Article

                Public health
                adolescent,metabolic syndrome,dyslipidemia
                Public health
                adolescent, metabolic syndrome, dyslipidemia

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