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Abstract Title:

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

Abstract Source:

PLoS One. 2016 ;11(1):e0145836. Epub 2016 Jan 26. PMID: 26812173

Abstract Author(s):

Esko Kemppainen, Jack George, Görkem Garipler, Tea Tuomela, Essi Kiviranta, Tomoyoshi Soga, Cory D Dunn, Howard T Jacobs

Article Affiliation:

Esko Kemppainen

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.

Study Type : Animal Study
Additional Links
Problem Substances : Glucose : CK(8) : AC(5)

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Sayer Ji
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