Mitochondrial Dysfunction Plus High-Sugar Diet Provokes a Metabolic Crisis That Inhibits Growth

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Kemppainen , E , George , J , Garipler , G , Tuomela , T , Kiviranta , E , Soga , T , Dunn , C D & Jacobs , H T 2016 , ' Mitochondrial Dysfunction Plus High-Sugar Diet Provokes a Metabolic Crisis That Inhibits Growth ' PLoS One , vol. 11 , no. 1 , 0145836 . DOI: 10.1371/journal.pone.0145836

Title: Mitochondrial Dysfunction Plus High-Sugar Diet Provokes a Metabolic Crisis That Inhibits Growth
Author: Kemppainen, Esko; George, Jack; Garipler, Görkem; Tuomela, Tea; Kiviranta, Essi; Soga, Tomoyoshi; Dunn, Cory D.; Jacobs, Howard T.
Contributor: University of Helsinki, Institute of Biotechnology
Date: 2016-01-26
Language: eng
Number of pages: 28
Belongs to series: PLoS One
ISSN: 1932-6203
URI: http://hdl.handle.net/10138/166062
Abstract: The Drosophila mutant tko(25t) exhibits a deficiency ofmitochondrial protein synthesis, leading to a global insufficiency of respiration and oxidative phosphorylation. This entrains an organismal phenotype of developmental delay and sensitivity to seizures induced bymechanical stress. We found that the mutant phenotype is exacerbated in a dose-dependent fashion by high dietary sugar levels. tko(25t) larvae were found to exhibit severe metabolic abnormalities that were further accentuated by high-sugar diet. These include elevated pyruvate and lactate, decreased ATP and NADPH. Dietary pyruvate or lactate supplementation phenocopied the effects of high sugar. Based on tissue-specific rescue, the crucial tissue in which this metabolic crisis initiates is the gut. It is accompanied by down-regulation of the apparatus of cytosolic protein synthesis and secretion at both the RNA and post-translational levels, including a novel regulation of S6 kinase at the protein level.
Subject: MITORIBOSOMAL PROTEIN S12
DROSOPHILA-MELANOGASTER
ALTERNATIVE OXIDASE
ESCHERICHIA-COLI
PYRUVATE THERAPY
KETOGENIC DIET
DISEASE
TRANSLATION
EXPRESSION
MUTATION
1182 Biochemistry, cell and molecular biology
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