ArticleScientific reports2016
Monotreme glucagon-like peptide-1 in venom and gut: one gene - two very different functions.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Toxins in disguise: Neuropeptide mimicry across animal venoms.General and comparative endocrinology · 2026Review
- Molecular mimicry: ecology, evolution, and applications of doppelgänger peptides.Trends in biochemical sciences · 2025Review
- Venom-derived peptides for breaking through the glass ceiling of drug development.Frontiers in chemistry · 2024Review
- Review
- Oral glucagon-like peptide 1 analogue ameliorates glucose intolerance in db/db mice.Biotechnology letters · 2022Article
- Unconventional insulins from predators and pathogens.Nature chemical biology · 2022Review
- Variation in the Evolution and Sequences of Proglucagon and the Receptors for Proglucagon-Derived Peptides in Mammals.Frontiers in endocrinology · 2021Article
- Insulin Release Mechanism Modulated by Toxins Isolated from Animal Venoms: From Basic Research to Drug Development Prospects.Molecules (Basel, Switzerland) · 2019Review
- Characterization of the Mel1c melatoninergic receptor in platypus (Ornithorhynchus anatinus).PloS one · 2018Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of Glucagon like peptide 1 (GLP-1) for metabolic control and insulin release sparked the evolution of genes mimicking GLP-1 action in venomous species (e.g. Exendin-4 in Heloderma suspectum (gila monster)). We discovered that platypus and echidna express a single GLP-1 peptide in both intestine and venom. Specific changes in GLP-1 of monotreme mammals result in resistance to DPP-4 cleavage which is also observed in the GLP-1 like Exendin-4 expressed in Heloderma venom. Remarkably we discovered that monotremes evolved an alternative mechanism to degrade GLP-1. We also show that monotreme GLP-1 stimulates insulin release in cultured rodent islets, but surprisingly shows low receptor affinity and bias toward Erk signaling. We propose that these changes in monotreme GLP-1 are the result of conflicting function of this peptide in metabolic control and venom. This evolutionary path is fundamentally different from the generally accepted idea that conflicting functions in a single gene favour duplication and diversification, as is the case for Exendin-4 in gila monster. This provides novel insight into the remarkably different metabolic control mechanism and venom function in monotremes and an unique example of how different selective pressures act upon a single gene in the absence of gene duplication.
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Registered trials
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