PEPCK-C reexpression in the liver counters neonatal hypoglycemia in Pck1del/del mice, unmasking role in non-gluconeogenic tissues
J. physiol. biochem
; 73(1): 89-98, feb. 2017. tab, ilus, graf
Article
em En
| IBECS
| ID: ibc-168396
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Localização: BNCS
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 (AU)
RESUMEN
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Base de dados:
IBECS
Assunto principal:
Fosfoenolpiruvato Carboxiquinase (GTP)
/
Erros Inatos do Metabolismo dos Carboidratos
/
Músculo Esquelético
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Hipoglicemia
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Fígado
/
Hepatopatias
/
Pulmão
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article