ArticleAging cell2019
Drosophila insulin-like peptide dilp1 increases lifespan and glucagon-like Akh expression epistatic to dilp2.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- A Tale of Two States: Similarities and Differences in Neuropeptide Signaling in Larval and Adult Drosophila.The Journal of comparative neurology · 2026Review
- Excess Sucrose in the Larval Diet Alters Gut Microbiota and Reduces Body Size and Longevity of Bactrocera dorsalis (Hendel).Neotropical entomology · 2026Article
- The cell autonomous and non-autonomous functions of Rab27 in longevity and neuroprotection inAutophagy · 2025Article
- Structure and activation of the Drosophila insulin receptor by three Drosophila insulin-like peptides.Nature communications · 2025Article
- Insulin/insulin-like growth factor signaling pathway promotes higher fat storage inbioRxiv : the preprint server for biology · 2025Article
- Mitochondrial Proteome Reveals Metabolic Tuning by Restricted Insulin Signaling to Promote Longevity inBiology · 2025Article
- Preventing excessive autophagy protects from the pathology of mtDNA mutations in Drosophila melanogaster.Nature communications · 2024Article
- Transcriptome Analysis Reveals Norathyriol Prolongs the Lifespan via Regulating Metabolism inMetabolites · 2024Article
- Transgenic sensors reveal compartment-specific effects of aggregation-prone proteins on subcellular proteostasis during aging.Cell reports methods · 2024Article
- Betulinic Acid Increases the Lifespan ofNutrients · 2024Article
- Kaempferol enhances intestinal repair and inhibits the hyperproliferation of aging intestinal stem cells inFrontiers in cell and developmental biology · 2024Article
- Diverse Regulatory Manners and Potential Roles of lncRNAs in the Developmental Process of Asian Honey Bee (International journal of molecular sciences · 2023Article
- Mechanisms of Neuroendocrine Stress Response inInsects · 2023Review
- Sex-biased gene expression in nutrient-sensing pathways.Proceedings. Biological sciences · 2023Article
- Quercetin Prevents Intestinal Stem Cell Aging via Scavenging ROS and Inhibiting Insulin Signaling inAntioxidants (Basel, Switzerland) · 2022Article
- Article
- Genome-wide analysis identifies Homothorax and Extradenticle as regulators of insulin in Drosophila Insulin-Producing cells.PLoS genetics · 2022Article
- Nutrient Sensing via Gut inInternational journal of molecular sciences · 2022Review
- Enhanced germline stem cell longevity in Drosophila diapause.Nature communications · 2022Article
- A mini-screen to identify the role of microRNAs in the Drosophila Insulin-Producing cells regulating lifespan.microPublication biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Insulin/IGF signaling (IIS) regulates essential processes including development, metabolism, and aging. The Drosophila genome encodes eight insulin/IGF-like peptide (dilp) paralogs, including tandem-encoded dilp1 and dilp2. Many reports show that longevity is increased by manipulations that decrease DILP2 levels. It has been shown that dilp1 is expressed primarily in pupal stages, but also during adult reproductive diapause. Here, we find that dilp1 is also highly expressed in adult dilp2 mutants under nondiapause conditions. The inverse expression of dilp1 and dilp2 suggests these genes interact to regulate aging. Here, we study dilp1 and dilp2 single and double mutants to describe epistatic and synergistic interactions affecting longevity, metabolism, and adipokinetic hormone (AKH), the functional homolog of glucagon. Mutants of dilp2 extend lifespan and increase Akh mRNA and protein in a dilp1-dependent manner. Loss of dilp1 alone has no impact on these traits, whereas transgene expression of dilp1 increases lifespan in dilp1 - dilp2 double mutants. On the other hand, dilp1 and dilp2 redundantly or synergistically interact to control circulating sugar, starvation resistance, and compensatory dilp5 expression. These interactions do not correlate with patterns for how dilp1 and dilp2 affect longevity and AKH. Thus, repression or loss of dilp2 slows aging because its depletion induces dilp1, which acts as a pro-longevity factor. Likewise, dilp2 regulates Akh through epistatic interaction with dilp1. Akh and glycogen affect aging in Caenorhabditis elegans and Drosophila. Our data suggest that dilp2 modulates lifespan in part by regulating Akh, and by repressing dilp1, which acts as a pro-longevity insulin-like peptide.
Indexed as
Identifiers
What OpenQuestion holds
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.