PEPCK-C reexpression in the liver counters neonatal hypoglycemia in Pck1del/del mice, unmasking role in non-gluconeogenic tissues

Jana Semakova, Petra Hyroššová, Andrés Méndez-Lucas, Ernest Cutz, Jordi Bermudez, Shawn Burgess, Soledad Alcántara, José C. Perales

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Whole body cytosolic phosphoenolpyruvate carboxykinase knockout (PEPCK-C KO) mice die early after birth with profound hypoglycemia therefore masking the role of PEPCK-C in adult, non-gluconeogenic tissues where it is expressed. To investigate whether PEPCK-C deletion in the liver was critically responsible for the hypoglycemic phenotype, we reexpress this enzyme in the liver of PEPCK-C KO pups by early postnatal administration of PEPCK-C-expressing adenovirus. This maneuver was sufficient to partially rescue hypoglycemia and allow the pups to survive and identifies the liver as a critical organ, and hypoglycemia as the critical pathomechanism, leading to early postnatal death in the whole-body PEPCK-C knockout mice. Pathology assessment of survivors also suggest a possible role for PEPCK-C in lung maturation and muscle metabolism.

Original languageEnglish (US)
Pages (from-to)1-10
Number of pages10
JournalJournal of Physiology and Biochemistry
DOIs
StateAccepted/In press - Oct 26 2016

Keywords

  • Gluconeogenesis
  • Hepatic lipidosis
  • KO
  • Liver
  • Neonatal hypoglycemia
  • PEPCK

ASJC Scopus subject areas

  • Physiology
  • Biochemistry

Fingerprint Dive into the research topics of 'PEPCK-C reexpression in the liver counters neonatal hypoglycemia in Pck1<sup>del/del</sup> mice, unmasking role in non-gluconeogenic tissues'. Together they form a unique fingerprint.

  • Cite this