Comparison of Different Definitions of Pediatric Metabolic Syndrome: Relation to Abdominal Adiposity, Insulin Resistance, Adiponectin, and Inflammatory Biomarkers

Division of Weight Management & Wellness, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
The Journal of pediatrics (Impact Factor: 3.79). 03/2008; 152(2):177-84. DOI: 10.1016/j.jpeds.2007.07.053
Source: PubMed


To examine the prevalence of the metabolic syndrome using different pediatric definitions reported in the literature and its relationship to abdominal adipose tissue (AT), in vivo insulin resistance, and inflammatory biomarkers in children and adolescents, as well as the utility of fasting insulin and adiponectin as predictors of the metabolic syndrome.
Cross-sectional measurements were obtained from 122 African Americans and 129 Caucasians age 8 to 19 years. Insulin sensitivity (IS) was measured by a 3-h hyperinsulinemic-euglycemic clamp. Blood pressure, fasting lipids, adiponectin, interleukin (IL)-6, adhesion molecules (intercellular adhesion molecule [ICAM]-1, vascular cell adhesion molecule [VCAM]-1, and E-selectin), and abdominal AT were measured.
Regardless of the metabolic syndrome criteria used, the prevalence of the metabolic syndrome was higher in overweight (24% approximately 51%) compared with non-overweight youths (1% approximately 3%) in both African Americans and Caucasians (P <.01). Youths with the metabolic syndrome had higher visceral AT and fasting insulin and lower IS and adiponetin independent of race (P < .01). In Caucasians, youths with the metabolic syndrome had higher levels of inflammatory biomarkers (IL-6, ICAM-1, and E-selectin). The area under the receiver operating curve (AUC) for insulin was 0.86 approximately 0.89 in African Americans and 0.86 approximately 0.89 in Caucasians, depending on the metabolic syndrome criteria used. For adiponetin, the AUC was 0.73 approximately 0.78 in African Americans and 0.81 approximately 0.86 in Caucasians.
The prevalence of metabolic syndrome varies depending on the definition used in the literature. Thus, there is a need for a unified definition of this syndrome in children and adolescents to streamline the research in this area. Independent of race, visceral obesity, insulin resistance, hyperinsulinemia, and hypoadiponectinemia are the common characteristics of youths with the metabolic syndrome. In Caucasians but not in African Americans, the metabolic syndrome is associated with increased inflammatory markers; however, the translation of such findings remains to be determined based on long-term longitudinal outcome studies in different racial groups.

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    • "These factors include central obesity, hypertension, hypertriglyceridemia, low HDL-cholesterol, and elevated fasting glucose [12] and show in increase in prevalence with age [13]. MetS appears to be associated with insulin resistance in adolescents in that increasing degrees of insulin resistance as determined by homeostasis model [14,15] and hyperinsulinemic clamp [16] are significantly associated with risk of MetS and/or its individual components. While the pathophysiology of T2DM consists of multiple overlying factors, including insulin resistance, excess hepatic glucose release and defects in adequate insulin production [17,18], the potential utility for MetS to identify risk in adolescents for future T2DM was demonstrated in that adolescents with MetS (compared to those without MetS) have an odds ratio (OR) of 10 for developing T2DM by age 32 [19]. "
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    ABSTRACT: The presence of impaired glucose tolerance (IGT) and metabolic syndrome (MetS) are two risk factors for Type 2 diabetes. The inter-relatedness of these factors among adolescents is unclear. We evaluated the sensitivity and specificity of MetS for identifying IGT in an unselected group of adolescents undergoing oral glucose tolerance tests (OGTT) in the National Health and Nutrition Evaluation Survey 1999-2010. We characterized IGT as a 2-hour glucose >=140 mg/dL and MetS using ATP-III-based criteria and a continuous sex- and race/ethnicity-specific MetS Z-score at cut-offs of +1.0 and +0.75 standard deviations (SD) above the mean. Among 1513 adolescents, IGT was present in 4.8 %, while ATP-III-MetS was present in 7.9 %. MetS performed poorly in identifying adolescents with IGT with a sensitivity/specificity of 23.7 %/92.9 % for ATP-III-MetS, 23.6 %/90.8 % for the MetS Z-score at +1.0 SD and 35.8 %/85.0 for the MetS Z-score at +0.75 SD. Sensitivity was higher (and specificity lower) but was still overall poor among overweight/obese adolescents: 44.7 %/83.0 % for ATP-III-MetS, 43.1 %/77.1 % for the MetS Z-score at +1.0 SD and 64.3 %/64.3 % for MetS Z-score at +0.75 SD. This lack of overlap between MetS and IGT may indicate that assessment of MetS is not likely to be a good indicator of which adolescents to screen using OGTT. These data further underscore the importance of other potential contributors to IGT, including Type 1 diabetes and genetic causes of poor beta-cell function. Practitioners should keep these potential causes of IGT in mind, even when evaluating obese adolescents with IGT.
    Cardiovascular Diabetology 04/2014; 13(1):83. DOI:10.1186/1475-2840-13-83 · 4.02 Impact Factor
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    • "We decided to use the OGTT instead of IVGTT because OGTT describes the post-meal dynamics which is of interest for the GH physiology being GH a hormone that principally acts in the post-absorptive phase [1]. Moreover, we chose the OGTT-derived indices of insulin sensitivity and secretion because they correlate well with clamp measures in children [44], [45], are easily calculated in epidemiological or intervention studies, and DI calculated by the OGTT has been demonstrated to predict diabetes development in adults [24]. Furthermore, the OGTT is the test that is classically performed in the clinical practice during rhGH treatment being simpler and cheaper than IVGTT. "
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    ABSTRACT: Growth hormone deficiency (GHD) is associated with insulin resistance and diabetes, in particular after treatment in children and adults with pre-existing metabolic risk factors. Our aims were. i) to evaluate the effect on glucose metabolism of rhGH treatment and withdrawal in not confirmed GHD adolescents at the achievement of adult height; ii) to investigate the impact of GH receptor gene genomic deletion of exon 3 (d3GHR). We performed a longitudinal study (1 year) in a tertiary care center. 23 GHD adolescent were followed in the last year of rhGH treatment (T0), 6 (T6) and 12 (T12) months after rhGH withdrawal with fasting and post-OGTT evaluations. 40 healthy adolescents were used as controls. HOMA-IR, HOMA%β, insulinogenic (INS) and disposition (DI) indexes were calculated. GHR genotypes were determined by multiplex PCR. In the group as a whole, fasting insulin (p<0.05), HOMA-IR (p<0.05), insulin and glucose levels during OGTT (p<0.01) progressively decreased from T0 to T12 becoming similar to controls. During rhGH, a compensatory insulin secretion with a stable DI was recorded, and, then, HOMAβ and INS decreased at T6 and T12 (p<0.05). By evaluating the GHR genotype, nDel GHD showed a decrease from T0 to T12 in HOMA-IR, HOMAβ, INS (p<0.05) and DI. Del GHD showed a gradual increase in DI (p<0.05) and INS with a stable HOMA-IR and higher HDL-cholesterol (p<0.01). In not confirmed GHD adolescents the fasting deterioration in glucose homeostasis during rhGH is efficaciously coupled with a compensatory insulin secretion and activity at OGTT. The presence of at least one d3GHR allele is associated with lower glucose levels and higher HOMA-β and DI after rhGH withdrawal. Screening for the d3GHR in the pediatric age may help physicians to follow and phenotype GHD patients also by a metabolic point of view.
    PLoS ONE 01/2014; 9(1):e87157. DOI:10.1371/journal.pone.0087157 · 3.23 Impact Factor
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    • "Childhood obesity is a serious public health problem that has reached epidemic proportions all over the world [1,2]. In children, the presence of obesity has been associated with increased levels of high sensitivity CRP (hsCRP) [3], as well as other inflammatory mediators [4-8], all of which promote the development of endothelial and metabolic dysfunction [9-12]. Serum amyloid A (SAA) is not only a sensitive acute phase proteins in plasma, but also an apolipoprotein that can replace apolipoprotein A1 (apoA1) as the major apolipoprotein of HDL-C, particularly during the acute phase response [13]. "
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    ABSTRACT: Obesity increases the risk for insulin resistance and metabolic syndrome in both adults and children. SAA is a member of apolipoprotein and plays an important role in maintaining glucose and lipid homeostasis. The purpose of this study was to assess SAA1 allelic variants with obesity in young school-age children. A total of 520 consecutive children ages 5--15 years were recruited. Children were divided based on BMI z score into Obese (OB; BMI z score >=1.65; n = 253) and non-obese (NOB; n = 267). Four SNPs of the human SAA1 gene (rs12218, rs4638289, rs7131332 and rs11603089) were genotyped by use of polymerase chain reaction -- restriction fragment length polymorphism (PCR-RFLP) method. Compared to NOB, circulating SAA levels were increased in OB, as were LDL-C, TG and TC concentration. Obese children showed increased frequency of rs12218 and rs4638289 polymorphism compared to control children. There were no differences between OB and NOB for the other 2 polymorphisms. Only the rs4638289 polymorphism showed significant contributions to higher SAA plasma levels. SAA1 genetic polymorphism was associated with obesity in Chinese children.
    Lipids in Health and Disease 10/2013; 12(1):161. DOI:10.1186/1476-511X-12-161 · 2.22 Impact Factor
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