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      A New Approach to Define and Diagnose Cardiometabolic Disorder in Children

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          Abstract

          The aim of the study was to test the performance of a new definition of metabolic syndrome (MetS), which better describes metabolic dysfunction in children. Methods. 15,794 youths aged 6–18 years participated. Mean z-score for CVD risk factors was calculated. Sensitivity analyses were performed to evaluate which parameters best described the metabolic dysfunction by analysing the score against independent variables not included in the score. Results. More youth had clustering of CVD risk factors (>6.2%) compared to the number selected by existing MetS definitions (International Diabetes Federation (IDF) < 1%). Waist circumference and BMI were interchangeable, but using insulin resistance homeostasis model assessment (HOMA) instead of fasting glucose increased the score. The continuous MetS score was increased when cardiorespiratory fitness (CRF) and leptin were included. A mean z-score of 0.40–0.85 indicated borderline and above 0.85 indicated clustering of risk factors. A noninvasive risk score based on adiposity and CRF showed sensitivity and specificity of 0.85 and an area under the curve of 0.92 against IDF definition of MetS. Conclusions. Diagnosis for MetS in youth can be improved by using continuous variables for risk factors and by including CRF and leptin.

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          Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation.

          K.G.M.M. Alberti, P.Z. Zimmet (1998)
          The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
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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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              Waist circumference percentiles in nationally representative samples of African-American, European-American, and Mexican-American children and adolescents.

              José R Fernández, David Redden, Angelo Pietrobelli … (2004)
              To describe and provide estimates of the distribution of waist circumference (WC) according to percentiles in African-, European-, and Mexican-American children, and to test for group differences at different percentiles. Cross-sectional data from the Third National Health and Nutrition Examination Survey (NHANES III) were examined. The sample evaluated included 9713 nonpregnant persons 2 to 18 years of age with measured values of WCs. Age-, sex-, and ethnicity-specific percentiles were estimated via percentile regression. WC measurements increased in a monotonic fashion across ages but at nonconstant rates and in a manner that varied across age and sex. At higher percentiles of the distribution, estimates of WC differ between Mexican-American (MA) and European-American (EA) and between African-American (AA) and European-American (EA), and, in some cases, exceeded the adult cutoff value for obesity-related disease risk at as early as 13 years of age. Age-, sex-, and ethnicity-specific WC percentiles are available for US children and adolescents and can be used as an assessment tool that could impact public health recommendations. Results suggest concern with respect to high WC values among certain ethnic groups.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date (Print): 2015
                Publication date (Electronic): 6 April 2015
                Volume: 2015
                Electronic Location Identifier: 539835
                Affiliations
                1Center of Research in Childhood Health, Department of Sport Sciences and Clinical Biomechanics, University of Southern Denmark, Campusvej 55, 5230 Odense M, Denmark
                2Department of Sports Medicine, Norwegian School of Sport Sciences, Sognsveien 220, 0806 Oslo, Norway
                3Exercise and Health Laboratory, CIPER, Fac Motricidade Humana, Universidade de Lisboa, Estrada Dacosth, Cruz-Quebrada, 1499 Lisbon, Portugal
                4Department of Exercise and Sport Science, University of North Carolina, 025 Fetzer Gym, CB No. 8700, Chapel Hill, NC 27599-8700, USA
                5School of Physical Education, University of Pernambuco, Campus Universitario HUOC-ESEF, Arnobio Marques 310, Santo Amaro, 50.100-130 Recife, PE, Brazil
                6Epidemiology, Biostatistics and Prevention Institute, University of Zürich, Hirschengraben 84, 8001 Zürich, Switzerland
                7The Centre of Inflammation and Metabolism and Trygfondens Center for Aktiv Sundhed, Department of Infectious Diseases and CMRC, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Tagensvej 20, 2100 Copenhagen, Denmark
                8MRC Epidemiology Unit, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Hills Road, Cambridge CB2 0QQ, UK
                Author notes

                Academic Editor: Francesco Chiarelli

                Author information
                http://orcid.org/0000-0002-9800-029X
                Article
                DOI: 10.1155/2015/539835
                PMC ID: 4402570
                PubMed ID: 25945355
                SO-VID: f8cd986d-9183-41b8-b02c-1a0d5be28b2d
                Copyright © Copyright © 2015 Lars Bo Andersen et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 November 2014
                Date accepted : 17 March 2015
                Categories
                Subject: Research Article

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