Correction: Liver AMP-Activated Protein Kinase Is Unnecessary for Gluconeogenesis but Protects Energy State during Nutrient Deprivation
| Autor: | Martha L. Wall, David H. Wasserman, D. Emerson Ridley, Benoit Viollet, Curtis C. Hughey, Clinton M. Hasenour, E. Patrick Donahue, Marc Foretz, Jamey D. Young, Freyja D. James |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Multidisciplinary biology Anabolism Glycogen Catabolism Science AMPK Citric acid cycle 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology Endocrinology AMP-activated protein kinase chemistry Gluconeogenesis Internal medicine biology.protein medicine Medicine Citrate synthase |
| Zdroj: | PLoS ONE, Vol 12, Iss 8, p e0183601 (2017) |
| ISSN: | 1932-6203 |
| Popis: | AMPK is an energy sensor that protects cellular energy state by attenuating anabolic and promoting catabolic processes. AMPK signaling is purported to regulate hepatic gluconeogenesis and substrate oxidation; coordination of these processes is vital during nutrient deprivation or pathogenic during overnutrition. Here we directly test hepatic AMPK function in regulating metabolic fluxes that converge to produce glucose and energy in vivo. Flux analysis was applied in mice with a liver-specific deletion of AMPK (L-KO) or floxed control littermates to assess rates of hepatic glucose producing and citric acid cycle (CAC) fluxes. Fluxes were assessed in short and long term fasted mice; the latter condition is a nutrient stressor that increases liver AMP/ATP. The flux circuit connecting anaplerosis with gluconeogenesis from the CAC was unaffected by hepatic AMPK deletion in short and long term fasting. Nevertheless, depletion of hepatic ATP was exacerbated in L-KO mice, corresponding to a relative elevation in citrate synthase flux and accumulation of branched-chain amino acid-related metabolites. L-KO mice also had a physiological reduction in flux from glycogen to G6P. These results demonstrate AMPK is unnecessary for maintaining gluconeogenic flux from the CAC yet is critical for stabilizing liver energy state during nutrient deprivation. |
| Databáze: | OpenAIRE |
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