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PTP1B deficiency enhances liver growth during suckling by increasing the expression of insulin-like growth factor-I

Fernando Escrivá1, Agueda González-Rodriguez, Elisa Fernández-Millán

  • 1Centro de Investigación Biomédica en Red de Diabetes y Enferemdades Metabólicas Asociadas, Instituto de Salud Carlos III, Madrid, Spain.

Journal of Cellular Physiology
|May 28, 2010
PubMed

Insights

Protein tyrosine phosphatase 1B (PTP1B) deficiency enhances neonatal liver growth and glucose metabolism via the pentose phosphate pathway. This suggests PTP1B uniquely controls early liver development.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Developmental Biology

Background:

  • Protein tyrosine phosphatase 1B (PTP1B) negatively regulates insulin and growth factor signaling.
  • Previous studies showed PTP1B deficiency impacts glucose uptake in neonatal hepatocytes.

Purpose of the Study:

  • Investigate the role of PTP1B in intrahepatic glucose utilization and liver development in neonatal mice.
  • Determine the molecular mechanisms underlying PTP1B's effects on neonatal liver physiology.

Main Methods:

  • Comparative analysis of wild-type and PTP1B(-/-) neonatal mice (3-5 days old).
  • Biochemical assays for glycogen, lactate, pyruvate, and triglyceride content.
  • Enzyme activity assays (G6PD).
  • Molecular analyses including gene and protein expression (STAT 5B, IGF-I, IGF-IR, PCNA).
  • Embryo transfer experiments to assess maternal vs. embryonic PTP1B roles.

Main Results:

  • PTP1B deficiency decreased liver glycogen, lactate, and pyruvate but increased glucose 6-phosphate dehydrogenase (G6PD) activity in neonatal mice.
  • Enhanced STAT 5B phosphorylation, IGF-I signaling, and PCNA expression were observed in PTP1B-deficient livers.
  • Increased liver weight, DNA content, and liver-to-body mass ratio in PTP1B(-/-) neonates.
  • Elevated hepatic and serum triglycerides in PTP1B(-/-) mice, linked to maternal milk composition.
  • Embryo transfer studies indicated maternal PTP1B influences neonatal fat accumulation, but not liver growth or metabolic changes.

Conclusions:

  • PTP1B plays a critical role in regulating neonatal liver development and glucose metabolism.
  • PTP1B deficiency promotes liver growth and alters metabolic pathways through effects on G6PD and the IGF-I axis.
  • Maternal PTP1B influences neonatal hepatic fat accumulation, suggesting a complex interplay between maternal and embryonic factors.

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