ArticlePloS one2016
Mitochondrial Dysfunction Plus High-Sugar Diet Provokes a Metabolic Crisis That Inhibits Growth.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Pathological Role of High Sugar in Mitochondrial Respiratory Chain Defect-Augmented Mitochondrial Stress.Biology · 2024Article
- Nuclear genetic background influences the phenotype of the Drosophila tko25t mitochondrial protein-synthesis mutant.G3 (Bethesda, Md.) · 2023Article
- Regulation of growth in Drosophila melanogaster: the roles of mitochondrial metabolism.Journal of biochemistry · 2020Review
- Review
- Minimal effects ofBiology open · 2019Article
- Lethal Interaction of Nuclear and Mitochondrial Genotypes inG3 (Bethesda, Md.) · 2019Article
- Alternative oxidase confers nutritional limitation on Drosophila development.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2019Article
- Shortened Lifespan and Other Age-Related Defects in Bang Sensitive Mutants ofG3 (Bethesda, Md.) · 2018Article
- Article
- Genotype to phenotype: Diet-by-mitochondrial DNA haplotype interactions drive metabolic flexibility and organismal fitness.PLoS genetics · 2018Review
- Mitochondrial Dysfunction and Infection Generate Immunity-Fecundity Tradeoffs in Drosophila.Integrative and comparative biology · 2018Article
- Regulation of Carbohydrate Energy Metabolism inGenetics · 2017Review
- Adaptation to dietary conditions by trehalose metabolism in Drosophila.Scientific reports · 2017Article
- Insights into pancreatic β cell energy metabolism using rodent β cell models.Wellcome open research · 2017Article
- Correction: Mitochondrial Dysfunction Plus High-Sugar Diet Provokes a Metabolic Crisis That Inhibits Growth.PloS one · 2016Article
- Reduced Glucose Sensation Can Increase the Fitness of Saccharomyces cerevisiae Lacking Mitochondrial DNA.PloS one · 2016Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Drosophila mutant tko25t exhibits a deficiency of mitochondrial 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 by mechanical stress. We found that the mutant phenotype is exacerbated in a dose-dependent fashion by high dietary sugar levels. tko25t 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.