期刊
JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
卷 73, 期 1, 页码 89-98出版社
SPRINGER
DOI: 10.1007/s13105-016-0528-y
关键词
PEPCK; Gluconeogenesis; Liver; Neonatal hypoglycemia; KO; Hepatic lipidosis
资金
- Ministerio de Economia y Competitividad
- FEDER [BFU2012-37177, BFU2015-66030-R]
- Ministerio de Educacion y Ciencia
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-Cexpressing 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.
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