ArticleDisease models & mechanisms2013
Altered lipid homeostasis in Drosophila InsP3 receptor mutants leads to obesity and hyperphagia.
Article in Disease models & mechanisms, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
- Lipid Metabolism in Relation to Calcium Homeostasis.Advances in experimental medicine and biology · 2026Review
- Gut microbiota metabolite tyramine ameliorates high-fat diet-induced insulin resistance via increased CaThe EMBO journal · 2024Article
- The integral role of de novo lipogenesis in the preparation for seasonal dormancy.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- Viruses in LaboratoryViruses · 2023Article
- Molecular Changes in Cells of Patients with Type 2 Diabetes Mellitus Depending on Changes in Glycemia Level in the Context of Lifestyle-An Overview of the Latest Scientific Discoveries.Current issues in molecular biology · 2023Review
- Inositol in Disease and Development: Roles of Catabolism viaInternational journal of molecular sciences · 2023Article
- MS4A15 drives ferroptosis resistance through calcium-restricted lipid remodeling.Cell death and differentiation · 2022Article
- Genetic polymorphisms of CaFrontiers in endocrinology · 2022Article
- Emerging Roles of Calcium Signaling in the Development of Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2021Review
- Aberrant CaScience signaling · 2021Article
- Adipocyte CAMK2 deficiency improves obesity-associated glucose intolerance.Molecular metabolism · 2021Article
- Predicting novel candidate human obesity genes and their site of action by systematic functional screening in Drosophila.PLoS biology · 2021Article
- A Comparative Perspective on Functionally-Related, Intracellular Calcium Channels: The Insect Ryanodine and Inositol 1,4,5-Trisphosphate Receptors.Biomolecules · 2021Review
- ERp44/CG9911 promotes fat storage inAging · 2021Article
- What You Eat Matters: Nutrient Inputs Alter the Metabolism and Neuropeptide Expression in Egyptian Cotton Leaf Worm,Frontiers in physiology · 2021Article
- Article
- Tissue-specific analysis of lipid species inJournal of lipid research · 2020Article
- The Mitochondrial CaFrontiers in physiology · 2020Review
- The Role of Peptide Hormones in Insect Lipid Metabolism.Frontiers in physiology · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Obesity is a complex metabolic disorder that often manifests with a strong genetic component in humans. However, the genetic basis for obesity and the accompanying metabolic syndrome is poorly defined. At a metabolic level, obesity arises from an imbalance between the nutritional intake and energy utilization of an organism. Mechanisms that sense the metabolic state of the individual and convey this information to satiety centers help achieve this balance. Mutations in genes that alter or modify such signaling mechanisms are likely to lead to either obese individuals, who in mammals are at high risk for diabetes and cardiovascular disease, or excessively thin individuals with accompanying health problems. Here we show that Drosophila mutants for an intracellular calcium signaling channel, the inositol 1,4,5-trisphosphate receptor (InsP3R) store excess triglycerides in their fat bodies and become unnaturally obese on a normal diet. Although excess insulin signaling can rescue obesity in InsP3R mutants to some extent, we show that it is not the only cause of the defect. Through mass spectrometric analysis of lipids we find that homeostasis of storage and membrane lipids are altered in InsP3R mutants. Possibly as a compensatory mechanism, InsP3R mutant adults also feed excessively. Thus, reduced InsP3R function alters lipid metabolism and causes hyperphagia in adults. Together, the metabolic and behavioral changes lead to obesity. Our results implicate altered InsP3 signaling as a previously unknown causative factor for metabolic syndrome in humans. Importantly, our studies also suggest preventive dietary interventions.
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