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Novel measures of inflammation and insulin resistance are related to obesity and fitness in a diverse sample of 11–14 year-olds: The HEALTHY Study

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      GlycA is a novel serum marker of systemic inflammation. There is no information on GlycA in pediatric populations, how it differs by gender or its association with body mass index (BMI) or fitness. LP-IR is a serum measure of insulin resistance which is related to changes in BMI group in adolescents, but its relationship with fitness is unknown. The current study examined the independent associations between fitness and BMI with GlycA and LP-IR among US adolescents.


      Participants were 1664 US adolescents from the HEALTHY study with complete 6 th and 8 th grade BMI, fitness and blood data. GlycA and LP-IR were measured by NMR spectroscopy. Three BMI groups and three fitness groups were created. Linear mixed models examined associations between GlycA, LP-IR, fitness and BMI.


      LP-IR decreased between 6 th and 8 th grade. GlycA increased among girls but decreased among boys. At 8 th grade, median GlycA values were 27 (7.6%) μmol/L higher (381 versus 354) for girls than boys. Median GlycA 6 th grade values were 9% higher in obese girls than healthy weight girls. Overall there was strong evidence (p<0.001) that GlycA was higher in higher BMI groups. Fitness was negatively associated with GlycA (r = −0.37 and −0.35) and LP-IR (r = −0.34 and − 0.18) at the 6 th and 8 th grade assessments. As BMI category increased and fitness category decreased, GlycA and LP-IR levels increased. Lowest GlycA was found in the low BMI/high fitness group.


      GlycA was associated with BMI and fitness among in US adolescents. These findings suggest that there are independent effects for BMI and fitness group with both GlycA and LP-IR. Future studies should validate the role of GlycA and LP-IR to evaluate the effects of interventions to modify obesity and fitness in order to improve systemic inflammation and insulin resistance.

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      Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.

      The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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          Predicting obesity in young adulthood from childhood and parental obesity.

          Childhood obesity increases the risk of obesity in adulthood, but how parental obesity affects the chances of a child's becoming an obese adult is unknown. We investigated the risk of obesity in young adulthood associated with both obesity in childhood and obesity in one or both parents. Height and weight measurements were abstracted from the records of 854 subjects born at a health maintenance organization in Washington State between 1965 and 1971. Their parents' medical records were also reviewed. Childhood obesity was defined as a body-mass index at or above the 85th percentile for age and sex, and obesity in adulthood as a mean body-mass index at or above 27.8 for men and 27.3 for women. In young adulthood (defined as 21 to 29 years of age), 135 subjects (16 percent) were obese. Among those who were obese during childhood, the chance of obesity in adulthood ranged from 8 percent for 1- or 2-year-olds without obese parents to 79 percent for 10-to-14-year-olds with at least one obese parent. After adjustment for parental obesity, the odds ratios for obesity in adulthood associated with childhood obesity ranged from 1.3 (95 percent confidence interval, 0.6 to 3.0) for obesity at 1 or 2 years of age to 17.5 (7.7 to 39.5) for obesity at 15 to 17 years of age. After adjustment for the child's obesity status, the odds ratios for obesity in adulthood associated with having one obese parent ranged from 2.2 (95 percent confidence interval, 1.1 to 4.3) at 15 to 17 years of age to 3.2 (1.8 to 5.7) at 1 or 2 years of age. Obese children under three years of age without obese parents are at low risk for obesity in adulthood, but among older children, obesity is an increasingly important predictor of adult obesity, regardless of whether the parents are obese. Parental obesity more than doubles the risk of adult obesity among both obese and nonobese children under 10 years of age.

            Author and article information

            [1 ]Centre for Exercise, Nutrition & Health, School for Policy Studies, University of Bristol
            [2 ]The George Washington University Biostatistics Center
            [3 ]Laboratory Corporation of America
            [4 ]Children’s Hospital of Philadelphia & Perelman School of Medicine of the University of Pennsylvania
            [5 ]University of North Carolina School of Medicine
            Author notes
            Address for correspondence: Russell Jago PhD, Centre for Exercise, Nutrition and Health, School for Policy Studies, University of Bristol, 8 Priory RD, Bristol BS8 1TZ, UK. russ.jago@ , Tel: 44 (0) 117 9546603, Fax: 44(0) 117 3310418
            Int J Obes (Lond)
            Int J Obes (Lond)
            International journal of obesity (2005)
            26 April 2016
            04 May 2016
            July 2016
            04 November 2016
            : 40
            : 7
            : 1157-1163
            27143035 4935612 10.1038/ijo.2016.84 NIHMS780570

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