A1 Refereed original research article in a scientific journal

A diabetes-like biochemical and behavioural phenotype of Drosophila induced by predator stress




AuthorsKrama Tatjana, Bahhir Diana, Ots Liina, Popovs Sergejs, Bartkevičs Vadims, Pugajeva Iveta, Krams Ronalds, Merivee Enno, Must Anne, Rantala Markus J., Krams Indrikis, Jõers Priit

PublisherROYAL SOC

Publication year2023

JournalProceedings of the Royal Society B: Biological Sciences

Journal name in sourcePROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES

Journal acronymP ROY SOC B-BIOL SCI

Article number 20230442

Volume290

Issue2002

Number of pages10

ISSN0962-8452

eISSN1471-2954

DOIhttps://doi.org/10.1098/rspb.2023.0442

Web address https://doi.org/10.1098/rspb.2023.0442

Self-archived copy’s web addresshttps://research.utu.fi/converis/portal/detail/Publication/180704698


Abstract
Predation can have both lethal and non-lethal effects on prey. The non-lethal effects of predation can instil changes in prey life history, behaviour, morphology and physiology, causing adaptive evolution. The chronic stress caused by sustained predation on prey is comparable to chronic stress conditions in humans. Conditions like anxiety, depression, and post-traumatic stress syndrome have also been implicated in the development of metabolic disorders such as obesity and diabetes. In this study, we found that predator stress induced during larval development in fruit flies Drosophila melanogaster impairs carbohydrate metabolism by systemic inhibition of Akt protein kinase, which is a central regulator of glucose uptake. However, Drosophila grown with predators survived better under direct spider predation in the adult phase. Administration of metformin and 5-hydroxytryptophan (5-HTP), a precursor of the neurotransmitter serotonin, reversed these effects. Our results demonstrate a direct link between predator stress and metabolic impairment, suggesting that a diabetes-like biochemical phenotype may be adaptive in terms of survival and reproductive success. We provide a novel animal model to explore the mechanisms responsible for the onset of these metabolic disorders, which are highly prevalent in human populations.

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