| Literature DB >> 25937276 |
Anja Zeigerer1, Roman L Bogorad2, Kirti Sharma3, Jerome Gilleron4, Sarah Seifert1, Susanne Sales1, Nikolaus Berndt5, Sascha Bulik5, Giovanni Marsico6, Rochelle C J D'Souza3, Naharajan Lakshmanaperumal1, Kesavan Meganathan7, Karthick Natarajan7, Agapios Sachinidis7, Andreas Dahl8, Hermann-Georg Holzhütter5, Andrej Shevchenko1, Matthias Mann3, Victor Koteliansky9, Marino Zerial10.
Abstract
The liver maintains glucose and lipid homeostasis by adapting its metabolic activity to the energy needs of the organism. Communication between hepatocytes and extracellular environment via endocytosis is key to such homeostasis. Here, we addressed the question of whether endosomes are required for gluconeogenic gene expression. We took advantage of the loss of endosomes in the mouse liver upon Rab5 silencing. Strikingly, we found hepatomegaly and severe metabolic defects such as hypoglycemia, hypercholesterolemia, hyperlipidemia, and glycogen accumulation that phenocopied those found in von Gierke's disease, a glucose-6-phosphatase (G6Pase) deficiency. G6Pase deficiency alone can account for the reduction in hepatic glucose output and glycogen accumulation as determined by mathematical modeling. Interestingly, we uncovered functional alterations in the transcription factors, which regulate G6Pase expression. Our data highlight a requirement of Rab5 and the endosomal system for the regulation of gluconeogenic gene expression that has important implications for metabolic diseases.Entities:
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Year: 2015 PMID: 25937276 DOI: 10.1016/j.celrep.2015.04.018
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423