CIDeRplusGeneral Information:
| Id: | 6,415 (click here to show other Interactions for entry) |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance |
| Mus musculus | |
| article | |
| Reference: | Mendez-Lucas A et al.(2013) PEPCK-M expression in mouse liver potentiates, not replaces, PEPCK-C mediated gluconeogenesis J. Hepatol. 59: 105-113 [PMID: 23466304] |
Interaction Information:
| Comment | Phosphoenolpyruvate carboxykinase (PEPCK) (GTP; EC 4.1.1.32) catalyzes the conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP). Its activity is distributed both in the cytosol and mitochondria as a result of two enzymatically indistinct isozymes, PEPCK-C and PEPCK-M, encoded by different nuclear genes (Pck1 and Pck2, respectively). Liver-specific deletion of cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C) abolishes gluconeogenesis from mitochondrial substrates, deregulates lipid metabolism and affects TCA cycle. While the mouse liver almost exclusively expresses PEPCK-C, humans equally present a mitochondrial isozyme (PEPCK-M). PEPCK-M expression partially rescued defects in lipid metabolism, gluconeogenesis and TCA cycle function impaired by PEPCK-C deletion, while 10% re-expression of PEPCK-C normalized most parameters. When PEPCK-M was expressed in the presence of PEPCK-C, the mitochondrial isozyme amplified total gluconeogenic capacity, suggesting autonomous regulation of oxaloacetate to phosphoenolpyruvate fluxes by the individual isoforms. |
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Formal Description Interaction-ID: 60469 |
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