title: Leptin levels are strongly correlated with those of GH-binding protein in prepubertal children.
abstract: OBJECTIVE
  Nutritional status is an important determinant of growth, and previous studies have indicated that this is due, at least in part, to an increased target-tissue sensitivity to GH. An attractive candidate for mediating this effect is leptin, a hormone secreted by the adipose tissue. The aim of this study was to investigate if there was a connection between GH-binding protein (GHBP) and leptin.
  
  
  METHODS
  We investigated the relationship between serum levels of leptin and those of GHBP in 229 prepubertal children. These included 107 healthy children with normal GH secretion, 55 GH-deficient (GHD) children and 55 children born small for gestational age (SGA) sampled on one occasion for GHBP and leptin, and 12 healthy children followed longitudinally at monthly interval for 1 year.
  
  
  RESULTS
  In the healthy children and in those born SGA, the serum concentration of GHBP was positively correlated with that of leptin (r = 0.65, P < 0.001; r = 0.74, P < 0.001 respectively). There was no correlation between GHBP and leptin in the group of children with GHD (r = 0.27, not significant). This means that leptin alone explained 42% of the variation of GHBP in the healthy group and 55% in the SGA group. The correlation remained after adjustment for body mass index and age in the healthy children (r = 0.57, P < 0.0001, r2 = 0.33) and for children born SGA (r = 0.74, P < 0.0001, r2 = 0.55). There was a positive correlation between the intra-individual monthly changes in GHBP and changes in leptin respectively, in the 12 healthy children followed longitudinally, the mean of the correlation coefficients was 0.38 (median = 0.29; range 0.03 to 0.86; P < 0.05).
  
  
  CONCLUSIONS
  There was a highly significant correlation between serum levels of leptin and those of GHBP, except in children with GHD. The possibility that leptin could mediate the effects of body fat mass on GH sensitivity, therefore, merits further investigation.
authors.affiliation: Department of Pediatrics, Sahlgrenska University Hospital, University of Göteborg, Sweden.
authors.forename: R
authors.initials: R
authors.lastname: Bjarnason
authors.forename: M
authors.initials: M
authors.lastname: Boguszewski
authors.forename: J
authors.initials: J
authors.lastname: Dahlgren
authors.forename: L
authors.initials: L
authors.lastname: Gelander
authors.forename: B
authors.initials: B
authors.lastname: Kriström
authors.forename: S
authors.initials: S
authors.lastname: Rosberg
authors.forename: B
authors.initials: B
authors.lastname: Carlsson
authors.forename: K
authors.initials: K
authors.lastname: Albertsson-Wikland
authors.forename: L M
authors.initials: LM
authors.lastname: Carlsson
mesh_terms: D000293:Adolescent; D015992:Body Mass Index; D002352:Carrier Proteins / Q000097:blood*; D002648:Child; D002675:Child, Preschool; D003430:Cross-Sectional Studies; D005260:Female; D019382:Human Growth Hormone / Q000172:deficiency / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D020738:Leptin; D008137:Longitudinal Studies; D008297:Male; D011506:Proteins / Q000378:metabolism*; D011627:Puberty; D012016:Reference Values
chemical_list: D002352:Carrier Proteins; D020738:Leptin; D011506:Proteins; D019382:Human Growth Hormone; C051815:somatotropin-binding protein