Involvement of the skeletal GH-IGF system in an experimental model of diabetes-induced growth retardation

Y. Segev*, D. Landau, S. Davidoff-Friedman, M. Weinreb, M. Phillip

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Uncontrolled diabetes is associated with growth retardation. We investigated the effect of insulin-dependent diabetes on animal growth and IGF-I gene expression in the epiphyseal growth plate region of the long bones. We also studied the effect of GH administration on somatic growth in the diabetic state. Streptozotocin (STZ)-injected diabetic rats had a decreased somatic growth rate in comparison to controls. GH administration (2.5 U/kg day) in the diabetic animals (DGH group) prevented this decrease. Serum IGF-I levels were decreased in both diabetic and DGH animals. Within 72 h from diabetes onset, IGF-I mRNA levels in epiphyseal growth plate homogenates decreased whereas IGF-I receptor mRNA levels increased in diabetic animals. The decrease in IGF-I mRNA transcript levels was localized to the metaphyseal region by in situ hybridization. We conclude that in the STZ-induced diabetic state, the reduction in linear growth is associated with a parallel decrease in IGF-I gene expression at the epiphyseal growth plate area. Diabetic growth retardation can be reversed with GH administration, which does not reconstitute serum IGF-I levels. Therefore, we speculate that GH in this model may act locally through the skeletal GH-IGF-I system.

Original languageEnglish
Pages (from-to)61-67
Number of pages7
JournalActa Diabetologica
Volume39
Issue number2
DOIs
StatePublished - 2002

Keywords

  • Diabetes, insulin-dependent
  • Growth
  • Growth hormone
  • Growth plate
  • Insulin-like growth factor-I

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