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Submitted on December 8, 2006
Accepted on February 27, 2007
Nemours Children's Clinic & Mayo Clinic College of Medicine, Jacksonville, FL; Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center & Harvard Medical School, Boston, MA
* To whom correspondence should be addressed. E-mail: bbalagop{at}nemours.org.
Context: Retinol binding protein (RBP4), secreted primarily from the liver and adipose tissues, was recently proposed as a link between obesity and insulin resistance. The role of RBP4 in pediatric obesity, its relationship with sub-clinical inflammation and its response to lifestyle changes are not elucidated.
Objective: To determine in children, (i) the status of RBP4 levels in lean vs obese; (ii) the relationship between RBP4 levels and sub-clinical inflammation and (iii) the effect of lifestyle-only intervention on RBP4 levels.
Design, Setting, and Patients: Lean and obese children (n=21) matched for age (>14 yrs<18 yrs) and maturity stage (Tanner IV) were studied at baseline and with lifestyle intervention in obese subjects only (n=15).
Intervention: Three months randomized and controlled physical activity-based lifestyle intervention.
Main outcome measure: RBP4 levels in children before and after intervention and the relationship between RBP4 and sub-clinical inflammation.
Results: Higher RBP4 levels in the obese group vs lean group (P=0.005). RBP4 correlated not only with indices of obesity and insulin resistance but also with inflammatory factors (r = 0.63 & 0.64 for CRP and IL-6 respectively, P < 0.01). Intervention reduced RBP4 levels by 
30% (P = 0.001) and RBP4 reduction was correlated with the magnitude of decrease in inflammatory factors (P = 0.01).
Conclusion: Alterations in serum RBP4 occur at an early age in the clinical course of obesity and appear to correlate with sub-clinical inflammation. Lifestyle intervention almost entirely reversed the raised RBP4 levels in obese children. Future studies should determine whether elevation of RBP4 is a direct trigger for the insulin resistance and sub-clinical inflammation implicated in the premature development of CVD and diabetes.
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