title: Erythrocyte insulin-like growth factor-L binding in younger and older males.
abstract: OBJECTIVE
  Insulin-like growth factor-1 (IGF-l) levels are lower in older compared with younger subjects. We tested the hypothesis that the reduction in circulating IGF-l would be accompanied by upregulation in tissue IGF-l binding in at least some tissues. We tested erythrocyte IGF-l binding since blood is an accessible tissue in humans, and there is growing evidence to suggest that erythrocyte IGF-l binding is influenced by circulating IGF-l.
  
  
  METHODS
  We compared 9 healthy older males (61-68 years old) with 9 healthy younger males (15-19 years old).
  
  
  METHODS
  Standard techniques were used to assay circulating IGF-l and IGF binding proteins 1-5 (IGFBPs 1-5). Erythrocyte IGF-l binding was first measured by studies in which native [125l]-IGF-l was displaced with unlabelled native IGF-l. In order to determine a possible role for IGF binding proteins (IGFBP), native [125l]-IGF-l was displaced with des-(1-3)IGF-1, which binds with IGF receptors but not IGFBPs.
  
  
  RESULTS
  As expected, circulating IGF-l was significantly lower in the older compared with the younger subjects. In addition, IGFBP-3 and 5 were significantly lower, and IGFBP-4 higher, in older compared with younger subjects. When native [125l]-IGF-l was displaced with unlabelled native IGF-l, the number of IGF-l binding sites per erythrocyte was higher in the older subjects (43 +/- 5 vs. 18 +/- 2, older vs. younger, respectively; P < 0.05). In contrast, when native [125l]-IGF-l was displaced with des-(1-3), IGF-l binding capacity was not different between the two age groups.
  
  
  CONCLUSIONS
  Erythrocyte IGF binding was increased in older compared with younger subjects. Surprisingly, the mechanism of the increase may not be a simple up regulation of IGF-l receptors in response to reduced circulating IGF-l, but possibly by an increase in the levels of as yet unidentified erythrocyte membrane-associated IGF binding proteins.
authors.affiliation: Department of Pediatrics, Harbor-UCLA Medical Center, Torrance.
authors.forename: D Y
authors.initials: DY
authors.lastname: Moromisato
authors.forename: C
authors.initials: C
authors.lastname: Roberts
authors.forename: J A
authors.initials: JA
authors.lastname: Brasel
authors.forename: S
authors.initials: S
authors.lastname: Mohan
authors.forename: E
authors.initials: E
authors.lastname: Cowles
authors.forename: S M
authors.initials: SM
authors.lastname: King
authors.forename: D M
authors.initials: DM
authors.lastname: Cooper
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000375:Aging / Q000378:metabolism*; D001665:Binding Sites; D004912:Erythrocytes / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood; D018974:Insulin-Like Growth Factor Binding Protein 4 / Q000097:blood; D018975:Insulin-Like Growth Factor Binding Protein 5 / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D011485:Protein Binding; D015854:Up-Regulation
chemical_list: D018972:Insulin-Like Growth Factor Binding Protein 3; D018974:Insulin-Like Growth Factor Binding Protein 4; D018975:Insulin-Like Growth Factor Binding Protein 5; D010446:Peptide Fragments; C058957:insulin-like growth factor 1, des-(1-3)-; D007334:Insulin-Like Growth Factor I