ArticleCell metabolism2010
High-fat-diet-induced obesity and heart dysfunction are regulated by the TOR pathway in Drosophila.
Article in Cell metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers.
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214 citing papers in PubMed, 391 citations in OpenAlex.
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- Metabolism fine tuning and cardiokines secretion represent adaptative responses of the heart to High Fat and High Sugar Diets in flies.PLoS genetics · 2026Article
- Cardiac neurons expressing a glucagon-like receptor mediate cardiac arrhythmia induced by high-fat diet ineLife · 2026Article
- Transcriptional Control of Lipid Metabolism.Advances in experimental medicine and biology · 2026Review
- Pachymic acid alleviates circadian rhythm disorders in high-fat diet-induced obesity mice via the sphingolipid pathway.PloS one · 2026Article
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- Preclinical research in obesity-associated metabolic diseases using in vitro, multicellular, and non-mammalian models.Journal of physiology and biochemistry · 2025Review
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- High-fat diet increases circulating palmitic acid produced by gut Bacteroides thetaiotaomicron to promote thrombosis.Cell reports. Medicine · 2025Article
- Microemulsion-based drug delivery system identifies pepper alkaloids as anti-obesity compounds.Acta pharmacologica Sinica · 2025Article
- High-fat diet impairs intermediate-term memory by autophagic-lysosomal dysfunction in Drosophila.PLoS genetics · 2025Article
- Insulin/insulin-like growth factor signaling pathway promotes higher fat storage inbioRxiv : the preprint server for biology · 2025Article
- Review
- Article
154 more citing papers are in PubMed but not listed here.
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9 authors at 1 institution in 1 country.
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Abstract
High-fat-diet (HFD)-induced obesity is a major contributor to diabetes and cardiovascular disease, but the underlying genetic mechanisms are poorly understood. Here, we use Drosophila to test the hypothesis that HFD-induced obesity and associated cardiac complications have early evolutionary origins involving nutrient-sensing signal transduction pathways. We find that HFD-fed flies exhibit increased triglyceride (TG) fat and alterations in insulin/glucose homeostasis, similar to mammalian responses. A HFD also causes cardiac lipid accumulation, reduced cardiac contractility, conduction blocks, and severe structural pathologies, reminiscent of diabetic cardiomyopathies. Remarkably, these metabolic and cardiotoxic phenotypes elicited by HFD are blocked by inhibiting insulin-TOR signaling. Moreover, reducing insulin-TOR activity (by expressing TSC1-2, 4EBP or FOXO), or increasing lipase expression-only within the myocardium-suffices to efficiently alleviate cardiac fat accumulation and dysfunction induced by HFD. We conclude that deregulation of insulin-TOR signaling due to a HFD is responsible for mediating the detrimental effects on metabolism and heart function.
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