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PERK eIF2alpha kinase regulates neonatal growth by controlling the expression of circulating insulin-like growth

Yulin Li1, Kaori Iida, Jeff O'Neil

  • 1Department of Biology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA.

Endocrinology
|July 17, 2003
PubMed

Insights

PERK deficiency causes severe growth retardation in neonatal mice by reducing liver IGF-I. This highlights PERK

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Developmental Biology

Background:

  • Wolcott-Rallison syndrome and PERK deficiency lead to severe postnatal growth retardation.
  • Perk-/- mice exhibit proportional dwarfism and reduced chondrocyte proliferation in growth plates.

Purpose of the Study:

  • Investigate the role of PERK in neonatal growth.
  • Determine the mechanism linking PERK deficiency to growth retardation.

Main Methods:

  • Analysis of growth parameters in Perk-/- mice.
  • Measurement of IGF-I mRNA and serum levels.
  • Assessment of growth hormone (GH) and IGF-I effects on growth retardation.
  • Transgenic rescue of PERK activity in beta-cells.

Main Results:

  • Perk-/- mice showed a 75% reduction in neonatal liver IGF-I mRNA and serum IGF-I.
  • IGF-I injections partially reversed growth retardation; GH had no effect.
  • PERK activity in beta-cells rescued juvenile but not neonatal growth.
  • Neonatal liver IGF-I is GH-independent.

Conclusions:

  • PERK regulates hepatic IGF-I expression during the GH-independent neonatal period.
  • PERK deficiency causes severe neonatal growth retardation due to impaired IGF-I regulation.
  • PERK is crucial for normal neonatal growth independent of GH signaling.

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