No relationship between leptin and cortisol in obese children and adolescents

Citation
K. Sudi et al., No relationship between leptin and cortisol in obese children and adolescents, J PED END M, 13(7), 2000, pp. 913-921
Citations number
27
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF PEDIATRIC ENDOCRINOLOGY & METABOLISM
ISSN journal
0334018X → ACNP
Volume
13
Issue
7
Year of publication
2000
Pages
913 - 921
Database
ISI
SICI code
0334-018X(200007/08)13:7<913:NRBLAC>2.0.ZU;2-N
Abstract
Recent findings have shown that leptin downregulates the steroid producing system in the adrenal. We studied the interactions of leptin, insulin and c ortisol in obese children and adolescents at different stages of maturation , In 44 boys (age 11 +/- 3.1 yr, body mass index [BMI] 29 +/- 5.3 [mean +/- SD]) and 35 girls (age 11.4 +/- 2.6 yr, BMI 29 +/- 4.3), blood levels of l eptin, insulin, cortisol, and glucose were determined. Fat mass (FM) was ca lculated by bioelectrical impedance. No significant differences were found between boys and girls with respect to humoral and anthropometric character istics. When children were divided according to maturation stage (prepubert al, pubertal, and late/postpubertal) insulin was higher in the more mature groups (p<0.01) and leptin was higher in the pubertal group (p=0.03). In th e prepubertal and pubertal groups, the expected positive relationship betwe en adiposity and leptin was found although the magnitude of this associatio n decreased with maturity. In none of the groups studied was cortisol signi ficantly correlated to leptin. Insulin (p=0.03) and glucose (p=0.01) were p ositively associated with cortisol in the prepubertal group after adjustmen t for adiposity. However, in the pubertal group an inverse correlation was found between insulin and cortisol (p=0.03), and between insulin and glucos e after control for adiposity. In the late/postpubertal group, no significa nt correlations were found between estimates of adiposity and humoral param eters even after adjustment for gender. Stepwise multiple regression failed to detect a significant influence of cortisol to explain the variation in leptin, and vice versa. BMI contributed to the variation in leptin (adj. R- 2=0.275, p<0.0001), and glucose added 5% to the variation in cortisol (p=0. 03). The results do not confirm the inverse association between leptin and cortisol found in adults. Although BMI reflects levels of leptin, it is lik ely that several ether factors in conjunction with fatness modulate the rel ationship with leptin. Whether leptin per se exerts an influence on the hyp othalamic-adrenal-adipo axis remains to be investigated in longitudinal stu dies.