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The effect of human growth hormone therapy on GH binding protein in GH-deficient children

Z Hochberg1, R J Barkey, L Even

  • 1Rappaport Family Institute for Research in The Medical Science, Technion, Haifa, Israel.

Acta Endocrinologica
|July 1, 1991
PubMed

Insights

Short-term human growth hormone (hGH) therapy in children with GH deficiency shows parallel increases in serum GH and GH binding protein. Long-term hGH treatment leads to elevated GH binding protein, suggesting receptor up-regulation.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Pediatrics

Background:

  • Growth hormone (GH) binding protein shares similarities with liver membrane GH receptors.
  • GH is known to regulate its own liver receptors.

Purpose of the Study:

  • To investigate the effects of short- and long-term human GH (hGH) therapy on GH binding protein in children with GH deficiency.
  • To understand the pharmacodynamics of serum GH and GH binding protein activity following initial hGH administration.

Main Methods:

  • Six GH-deficient children received their first hGH dose, with serum GH and GH binding protein activity monitored for 12 hours.
  • A second group of 7 GH-deficient patients with 30-36 months of hGH treatment were assessed.
  • Serum GH binding protein levels were measured before and during long-term hGH treatment.

Main Results:

  • Short-term hGH therapy showed a parallel increase in serum GH and GH binding protein activity for the first 6 hours, followed by a decrease.
  • A secondary peak in GH binding protein was observed in some patients at 8 hours, despite decreasing serum hGH.
  • Long-term hGH treatment (6 months and 30-36 months) resulted in progressively increased GH binding protein activity compared to pretreatment levels.

Conclusions:

  • Short-term changes in GH binding protein likely reflect endogenous GH receptor turnover.
  • Sustained elevation of GH binding protein during hGH treatment may indicate GH receptor up-regulation.
  • GH binding protein levels serve as a marker for GH receptor dynamics during therapy in GH-deficient children.

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