ArticleJournal of lipid research2016
CoA protects against the deleterious effects of caloric overload in Drosophila.
Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
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- Manipulation of pantothenate kinase in Anopheles stephensi suppresses pantothenate levels with minimal impacts on mosquito fitness.Insect biochemistry and molecular biology · 2022Article
- Loss of Stearoyl-CoA desaturase 1 leads to cardiac dysfunction and lipotoxicity.The Journal of experimental biology · 2021Article
- What You Eat Matters: Nutrient Inputs Alter the Metabolism and Neuropeptide Expression in Egyptian Cotton Leaf Worm,Frontiers in physiology · 2021Article
- Tissue-specific analysis of lipid species inJournal of lipid research · 2020Article
- Immune Control of Animal Growth in Homeostasis and Nutritional Stress inFrontiers in immunology · 2020Article
- Rumen Bacteria and Serum Metabolites Predictive of Feed Efficiency Phenotypes in Beef Cattle.Scientific reports · 2019Article
- Rapid metabolic shifts occur during the transition between hunger and satiety in Drosophila melanogaster.Nature communications · 2019Article
- Similar effects of high-fructose and high-glucose feeding in a Drosophila model of obesity and diabetes.PloS one · 2019Article
- Article
- Measurement of solid food intake in Drosophila via consumption-excretion of a dye tracer.Scientific reports · 2018Article
- Seven-Up Is a Novel Regulator of Insulin Signaling.Genetics · 2018Article
- A Complex Relationship between Immunity and Metabolism in Drosophila Diet-Induced Insulin Resistance.Molecular and cellular biology · 2018Article
- Review
- Regulation of Carbohydrate Energy Metabolism inGenetics · 2017Review
- Metabolomic Studies inGenetics · 2017Review
- Adaptation to dietary conditions by trehalose metabolism in Drosophila.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We developed a Drosophila model of T2D in which high sugar (HS) feeding leads to insulin resistance. In this model, adipose TG storage is protective against fatty acid toxicity and diabetes. Initial biochemical and gene expression studies suggested that deficiency in CoA might underlie reduced TG synthesis in animals during chronic HS feeding. Focusing on the Drosophila fat body (FB), which is specialized for TG storage and lipolysis, we undertook a series of experiments to test the hypothesis that CoA could protect against the deleterious effects of caloric overload. Quantitative metabolomics revealed a reduction in substrate availability for CoA synthesis in the face of an HS diet. Further reducing CoA synthetic capacity by expressing FB-specific RNAi targeting pantothenate kinase (PK orfumble) or phosphopantothenoylcysteine synthase (PPCS) exacerbated HS-diet-induced accumulation of FFAs. Dietary supplementation with pantothenic acid (vitamin B5, a precursor of CoA) was able to ameliorate HS-diet-induced FFA accumulation and hyperglycemia while increasing TG synthesis. Taken together, our data support a model where free CoA is required to support fatty acid esterification and to protect against the toxicity of HS diets.
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