ArticleNature communications2024
Fish-hunting cone snail disrupts prey's glucose homeostasis with weaponized mimetics of somatostatin and insulin.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed.
- From neuropeptides to toxins: illuminating the origins of venom complexity in cone snails.Molecular biology and evolution · 2026Article
- Toxins in disguise: Neuropeptide mimicry across animal venoms.General and comparative endocrinology · 2026Review
- Cone snail venom-inspired somatostatin receptor 4 (SSTRScientific reports · 2025Article
- From Neuropeptides to Toxins: Illuminating the Origins of Venom Complexity in Cone Snails.bioRxiv : the preprint server for biology · 2025Article
- Molecular mimicry: ecology, evolution, and applications of doppelgänger peptides.Trends in biochemical sciences · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Venomous animals have evolved diverse molecular mechanisms to incapacitate prey and defend against predators. Most venom components disrupt nervous, locomotor, and cardiovascular systems or cause tissue damage. The discovery that certain fish-hunting cone snails use weaponized insulins to induce hypoglycemic shock in prey highlights a unique example of toxins targeting glucose homeostasis. Here, we show that, in addition to insulins, the deadly fish hunter, Conus geographus, uses a selective somatostatin receptor 2 (SSTR
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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.