ArticlePLoS biology2018
Dietary rescue of lipotoxicity-induced mitochondrial damage in Peroxin19 mutants.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- The First Report of a Bang-Sensitive Strain inInternational journal of molecular sciences · 2026Article
- Toward a Unifying Hypothesis for Redesigned Lipid Catabolism as a Clinical Target in Advanced, Treatment-Resistant Carcinomas.International journal of molecular sciences · 2023Review
- Peroxisomal Stress Response and Inter-Organelle Communication in Cellular Homeostasis and Aging.Antioxidants (Basel, Switzerland) · 2022Review
- Drosophila Lipase 3 Mediates the Metabolic Response to Starvation and Aging.Frontiers in aging · 2022Article
- Loss of Stearoyl-CoA desaturase 1 leads to cardiac dysfunction and lipotoxicity.The Journal of experimental biology · 2021Article
- Current advances in the function and biogenesis of peroxisomes and their roles in health and disease.Histochemistry and cell biology · 2021Article
- Lauric acid alleviates insulin resistance by improving mitochondrial biogenesis in THP-1 macrophages.Molecular biology reports · 2020Article
- The Drosophila melanogaster as Genetic Model System to Dissect the Mechanisms of Disease that Lead to Neurodegeneration in Adrenoleukodystrophy.Advances in experimental medicine and biology · 2020Review
- Rosy Beginnings: Studying Peroxisomes inFrontiers in cell and developmental biology · 2020Review
- Peroxisomes: new insights into protein sorting, dynamics, quality control, signalling and roles in health and disease.Histochemistry and cell biology · 2019Article
- High fat diet induces sex-specific differential gene expression in Drosophila melanogaster.PloS one · 2019Article
- What Peroxisomes (Don't) do to Mitochondria.Contact (Thousand Oaks (Ventura County, Calif.))Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in peroxin (PEX) genes lead to loss of peroxisomes, resulting in the formation of peroxisomal biogenesis disorders (PBDs) and early lethality. Studying PBDs and their animal models has greatly contributed to our current knowledge about peroxisomal functions. Very-long-chain fatty acid (VLCFA) accumulation has long been suggested as a major disease-mediating factor, although the exact pathological consequences are unclear. Here, we show that a Drosophila Pex19 mutant is lethal due to a deficit in medium-chain fatty acids (MCFAs). Increased lipolysis mediated by Lipase 3 (Lip3) leads to accumulation of free fatty acids and lipotoxicity. Administration of MCFAs prevents lipolysis and decreases the free fatty acid load. This drastically increases the survival rate of Pex19 mutants without reducing VLCFA accumulation. We identified a mediator of MCFA-induced lipolysis repression, the ceramide synthase Schlank, which reacts to MCFA supplementation by increasing its repressive action on lip3. This shifts our understanding of the key defects in peroxisome-deficient cells away from elevated VLCFA levels toward elevated lipolysis and shows that loss of this important organelle can be compensated by a dietary adjustment.
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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.