PEPCK-M expression in mouse liver potentiates, not replaces, PEPCK-C mediated gluconeogenesis
Journal of Hepatology, ISSN: 0168-8278, Vol: 59, Issue: 1, Page: 105-113
2013
- 94Citations
- 111Captures
- 6Mentions
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Metrics Details
- Citations94
- Citation Indexes94
- 94
- CrossRef61
- Captures111
- Readers111
- 111
- Mentions6
- References6
- Wikipedia6
Article Description
Hepatic gluconeogenesis helps maintain systemic energy homeostasis by compensating for discontinuities in nutrient supply. 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). Despite clear relevance to human physiology, the role of PEPCK-M and its gluconeogenic potential remain unknown. Here, we test the significance of PEPCK-M in gluconeogenesis and TCA cycle function in liver-specific PEPCK-C knockout and WT mice.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0168827813001426; http://dx.doi.org/10.1016/j.jhep.2013.02.020; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84879142759&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/23466304; https://linkinghub.elsevier.com/retrieve/pii/S0168827813001426; http://www.journal-of-hepatology.eu/article/S0168-8278(13)00142-6/abstract; https://secure.jbs.elsevierhealth.com/action/getSharedSiteSession?redirect=http%3A%2F%2Fwww.journal-of-hepatology.eu%2Farticle%2FS0168-8278%2813%2900142-6%2Fabstract&rc=0&code=jhepat-site; http://acw.elsevier.com/SSOCore?return=https%3A%2F%2Fsecure.jbs.elsevierhealth.com%2Faction%2FconsumeSsoCookie%3FredirectUri%3Dhttp%253A%252F%252Fwww.journal-of-hepatology.eu%252Faction%252FconsumeSharedSessionAction%253FJSESSIONID%253Daaa_7fsyCzQ04-ZPgjnxv%2526MAID%253DArEdGYcIXsdYInKv9%25252B9EHA%25253D%25253D%2526SERVER%253DWZ6myaEXBLF%25252FdY29RpN4fA%25253D%25253D%2526ORIGIN%253D410096943%2526RD%253DRD; http://acw.elsevier.com/SSOCore/?return=https%3A%2F%2Fsecure.jbs.elsevierhealth.com%2Faction%2FconsumeSsoCookie%3FredirectUri%3Dhttp%253A%252F%252Fwww.journal-of-hepatology.eu%252Faction%252FconsumeSharedSessionAction%253FJSESSIONID%253Daaa_7fsyCzQ04-ZPgjnxv%2526MAID%253DArEdGYcIXsdYInKv9%25252B9EHA%25253D%25253D%2526SERVER%253DWZ6myaEXBLF%25252FdY29RpN4fA%25253D%25253D%2526ORIGIN%253D410096943%2526RD%253DRD; https://secure.jbs.elsevierhealth.com/action/consumeSsoCookie?redirectUri=http%3A%2F%2Fwww.journal-of-hepatology.eu%2Faction%2FconsumeSharedSessionAction%3FJSESSIONID%3Daaa_7fsyCzQ04-ZPgjnxv%26MAID%3DArEdGYcIXsdYInKv9%252B9EHA%253D%253D%26SERVER%3DWZ6myaEXBLF%252FdY29RpN4fA%253D%253D%26ORIGIN%3D410096943%26RD%3DRD&acw=&utt=; http://acw.elsevier.com/SSOCore?return=https%3A%2F%2Fsecure.jbs.elsevierhealth.com%2Faction%2FconsumeSsoCookie%3FredirectUri%3Dhttp%253A%252F%252Fwww.journal-of-hepatology.eu%252Faction%252FconsumeSharedSessionAction%253FJSESSIONID%253DaaaC02Fkp51A4hLPatTxv%2526MAID%253D2Rjq5p0PykzD37sdGKDXfw%25253D%25253D%2526SERVER%253DWZ6myaEXBLEIcey8uceZQQ%25253D%25253D%2526ORIGIN%253D296243893%2526RD%253DRD; http://acw.elsevier.com/SSOCore/?return=https%3A%2F%2Fsecure.jbs.elsevierhealth.com%2Faction%2FconsumeSsoCookie%3FredirectUri%3Dhttp%253A%252F%252Fwww.journal-of-hepatology.eu%252Faction%252FconsumeSharedSessionAction%253FJSESSIONID%253DaaaC02Fkp51A4hLPatTxv%2526MAID%253D2Rjq5p0PykzD37sdGKDXfw%25253D%25253D%2526SERVER%253DWZ6myaEXBLEIcey8uceZQQ%25253D%25253D%2526ORIGIN%253D296243893%2526RD%253DRD; https://secure.jbs.elsevierhealth.com/action/consumeSsoCookie?redirectUri=http%3A%2F%2Fwww.journal-of-hepatology.eu%2Faction%2FconsumeSharedSessionAction%3FJSESSIONID%3DaaaC02Fkp51A4hLPatTxv%26MAID%3D2Rjq5p0PykzD37sdGKDXfw%253D%253D%26SERVER%3DWZ6myaEXBLEIcey8uceZQQ%253D%253D%26ORIGIN%3D296243893%26RD%3DRD&acw=&utt=; http://linkinghub.elsevier.com/retrieve/pii/S0168827813001426
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