Down Syndrome Abstract
of the Month:
May 2008
Leptin levels among prepubertal children with Down syndrome compared with their siblings.
Magge SN, O'Neill KL, Shults J, Stallings VA, Stettler N.
J Pediatr. 2008 Mar;152(3):321-6
Division of Endocrinology and Diabetes, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
Abstract:
OBJECTIVES: To compare levels of leptin and other obesity-related hormones in prepubertal children with Down syndrome (DS), a population at high obesity risk, and those in unaffected siblings to better understand the pathophysiology of obesity in children with DS. STUDY DESIGN: This was a cross-sectional study of 35 children with DS and 33 control siblings, ages 4 to 10 years, with a fasting blood sample and anthropometric measurements to estimate body composition. Generalized estimating equations were used to account for the lack of independence between siblings. RESULTS: In addition to having higher body mass index and percent body fat, children with DS had higher leptin levels than unaffected siblings, even after adjustment for age, sex, race, and ethnicity (difference, 5.8 ng/mL; 95% CI, 2.4-9.3; P = .001) and further adjustment for percent body fat (difference, 2.7 ng/mL; 95% CI, 0.08-5.40, P = .04). Leptin and percent body fat were positively associated in both groups (P < .0001), but with a significantly greater positive association in the DS group, suggesting a significant effect modification (P < .0001). CONCLUSIONS: This group of children with DS had increased leptin levels for percent body fat than their unaffected siblings. This difference may contribute to the increased risk for obesity in children with DS.
My comments:
Leptin is a hormone that is made in fat cells (adipocytes) which then acts upon the hypothalamus to decrease appetite. The more leptin, the less hungry you are.This is a well-done study, with the researchers also looking at growth hormones, thyroid tests, and insulin levels to determine any differences between siblings. This is a small sample size, but the results show that there is more leptin in these children with DS than can be accounted for by their percentage of body fat measurements. Since the gene for coding leptin is found on the seventh chromosome, trisomy 21 cannot by itself account for this increase. There may be a defect in the feedback-stimulation loop involving the fat cells and the hypothalamus, but this is just conjecture at this point. But this study may be the first step to determining the reason for the high incidence of obesity in older children and adults with DS.
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