Adiposity Rebound and the Development of Metabolic Syndrome

PEDIATRICS (Impact Factor: 5.3). 12/2013; 133(1). DOI: 10.1542/peds.2013-0966
Source: PubMed

ABSTRACT OBJECTIVE:The age of adiposity rebound (AR) is defined as the time at which BMI starts to rise after infancy and is thought to be a marker of later obesity. To determine whether this age is related to future occurrence of metabolic syndrome, we investigated the relationship of the timing of AR with metabolic consequences at 12 years of age.METHODS:A total of 271 children (147 boys and 124 girls) born in 1995 and 1996 were enrolled in the study. Serial measurements of BMI were conducted at the ages of 4 and 8 months and 1, 1.5, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, and 12 years, based on which age of AR was calculated. Plasma lipids and blood pressure were measured at 12 years of age.RESULTS:An earlier AR (<4 years of age) was associated with a higher BMI (≥20) and a lipoprotein phenotype representative of insulin resistance. This phenotype consists of elevated triglycerides, apolipoprotein B, and atherogenic index and decreased high-density lipoprotein cholesterol in boys and elevated apolipoprotein B in girls at 12 years of age. The earlier AR was also related to elevated blood pressure in boys.CONCLUSIONS:This longitudinal population-based study indicates that children who exhibit AR at a younger age are predisposed to future development of metabolic syndrome. Therefore, monitoring of AR may be an effective method for the early identification of children at risk for metabolic syndrome.

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    ABSTRACT: To investigate whether increments of weight gain in early infancy are related to the timing of adiposity rebound (AR). A total of 271 children (147 boys and 124 girls) in 1 community were enrolled in the study. Serial measurements of body mass index were carried out at the ages of 4, 8, and 12 months and 1.5, 2, 3, 4, 5, 6, 7, 8, 9, and 10 years, based on which the age of AR was determined. We also calculated body weight increments in 3 separate periods: birth to 4 months, 4-8 months, and 8-12 months. There was no significant relationship between weight gain in any period of infancy and the age of AR. Weight gain between birth and 4 months was positively correlated only with body mass index at 7 years of age. We could not find an association between body weight gain during infancy and the timing of AR. This suggests that infantile weight gain is not related to childhood obesity through AR. Copyright © 2014 Elsevier Inc. All rights reserved.
    Journal of Pediatrics 11/2014; DOI:10.1016/j.jpeds.2014.10.003 · 3.74 Impact Factor
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    ABSTRACT: Evidence suggests that at a population level, childhood and adolescent obesity increase the long-term risk of chronic diseases such as type 2 diabetes and CVD. At an individual level, however, the metabolic consequences of obesity in youth vary immensely. Despite comparable BMI, some adolescents develop impaired glucose tolerance while others maintain normal glucose homeostasis. It has been proposed that the variation in the capacity to store lipid in the subcutaneous adipose tissue (SAT) may partially discriminate metabolically healthy from unhealthy obesity. In positive energy balance, a decreased capacity to expand SAT may drive lipid accumulation to visceral adipose tissue, liver and skeletal muscle. This state of lipotoxicity is associated with chronic low-grade inflammation, insulin resistance and dyslipidaemia. The present review examines the differential adipose tissue development and function in children and adolescents who exhibit metabolic dysregulation compared with those who are protected. Additionally, the role of manipulating dietary fat quality to potentially prevent and treat metabolic dysfunction in obesity will be discussed. The findings of the present review highlight the need for further randomised controlled trials to establish the effect of dietary n-3 PUFA on the metabolic phenotype of obese children and adolescents. Furthermore, using a personalised nutrition approach to target interventions to those at risk of, or those with established metabolic dysregulation may optimise the efficacy of modifying dietary fat quality.
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    ABSTRACT: OBJECTIVES: To investigate associations between timing of adiposity rebound (AR; the period in childhood where BMI begins to increase from its nadir) and adiposity (BMI, fat mass) at age 15 years in the Avon Longitudinal Study of Parents and Children (ALSPAC). METHODS: The sample consisted of 546 children with AR derived in childhood and BMI and fat mass index (FMI; fat mass measured by dual-energy radiograph absorptiometry/height in m(2)) measured at 15 years. Multivariable linear regression models were based on standardized residuals of log BMI and log FMI to allow comparison of regression coefficients across outcomes. RESULTS: There were strong dose-response associations between timing of AR and both adiposity outcomes at 15 years independent of confounders. BMI was markedly higher in adolescence for those with very early AR (by 3.5 years; beta = 0.70; 95% confidence interval [CI]: 0.33-1.07; P <= .001) and was also higher for those with early AR (between 3.5 and 5 years; beta = 0.34; 95% CI: 0.08-0.59; P = .009) compared with those with later AR (>5 years) after full adjustment for a range of potential confounders. Similar magnitudes of association were found for FMI after full adjustment for confounders (compared with later AR: very early AR beta = 0.74; 95% CI: 0.34-1.15; P <= .001; early AR beta = 0.35; 95% CI: 0.07-0.63; P = .02). CONCLUSIONS: Early AR is strongly associated with increased BMI and FMI in adolescence. Preventive interventions should consider targeting modifiable factors in early childhood to delay timing of AR.
    Pediatrics 10/2014; 134(5). DOI:10.1542/peds.2014-1908 · 5.30 Impact Factor