title: IGF-IR/ERK content and response to IGF-I and insulin in adipocytes from small for gestational age children.
abstract: OBJECTIVE
  The GH-IGF-I axis plays an important role on pre/postnatal growth in humans, and IGF-I regulates cell proliferation, differentiation, and metabolic homeostasis. The adipose tissue has an important function in energy storage, and plays an endocrine role through the production of several hormones and growth factors. There are few studies in humans regarding IGF-I and Insulin receptor signaling in adipocytes, particularly from AGA and SGA children.
  
  
  METHODS
  We studied 22 healthy prepubertal children (6.1+/-0.4 years), born at term (11 SGA and 11 AGA), and normal BMI at the time of the study. Primary cell cultures were established from subcutaneous adipose tissue biopsies. Preadipocytes were differentiated and stimulated with IGF-I or insulin and we studied IGF-IR, IR, AKT, and ERK content and phosphorylation.
  
  
  RESULTS
  The SGA children were shorter than the AGA children (height SDS -2.14+/-0.11 vs. 0.02+/-0.19, p<0.05). A lower content of IGF-IR, IR, AKT, and ERK was observed in adipocytes from SGA compared with AGA children. IGF-I stimulation increased IGF-IR and ERK phosphorylation in adipocytes from AGA, but not from SGA children.
  
  
  CONCLUSIONS
  The lower content and reduced phosphorylation of IGF-I signaling observed in adipocytes from SGA children may be related to the metabolic abnormalities described in these children.
authors.affiliation: Institute for Maternal and Child Research (IDIMI), School of Medicine, University of Chile, Santiago, Chile. giniguez@med.uchile.cl
authors.forename: German
authors.initials: G
authors.lastname: Iñiguez
authors.forename: Paulina
authors.initials: P
authors.lastname: Ormazabal
authors.forename: Teresa
authors.initials: T
authors.lastname: López
authors.forename: Diego
authors.initials: D
authors.lastname: Maldonado
authors.forename: Alejandra
authors.initials: A
authors.lastname: Avila
authors.forename: Rossana
authors.initials: R
authors.lastname: Román
authors.forename: Fernando
authors.initials: F
authors.lastname: Cassorla
mesh_terms: D017667:Adipocytes / Q000166:cytology / Q000187:drug effects*; D015153:Blotting, Western; D002648:Child; D005260:Female; D005865:Gestational Age; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age / Q000097:blood*; D007328:Insulin / Q000494:pharmacology*; D018972:Insulin-Like Growth Factor Binding Protein 3; D018969:Insulin-Like Growth Factor Binding Proteins / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D010766:Phosphorylation; D011627:Puberty / Q000097:blood; D017526:Receptor, IGF Type 1 / Q000378:metabolism*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood
chemical_list: D007004:Hypoglycemic Agents; C515497:IGFBP3 protein, human; D007328:Insulin; D018972:Insulin-Like Growth Factor Binding Protein 3; D018969:Insulin-Like Growth Factor Binding Proteins; D007334:Insulin-Like Growth Factor I; D013972:Thyrotropin; D017526:Receptor, IGF Type 1; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D013974:Thyroxine