The primary aim of this study was to analyse the influence of honeybee venom on various aspects of Drosophila melanogaster physiology and to assess the efficacy of adipokinetic hormone (AKH) in mitigating venom toxicity. We examined the harmful effects of venom on the thoracic muscles and central nervous system of Drosophila, as well as the potential use of AKH to counteract these effects. The results demonstrated that envenomation altered AKH levels in the Drosophila CNS, promoted cell metabolism, as evidenced by an increase in citrate synthase activity in muscles, and improved relative cell viability in both organs incubated in vitro. Furthermore, venom treatment reduced the activity of two key antioxidative stress enzymes, superoxide dismutase and catalase, and modified the expression of six genes encoding immune system components (Keap1, Relish, Nox, Eiger, Gadd45, and Domeless) in both organs. The venom also disrupted muscle cell ultrastructure, specifically myofibrils, and increased the release of arginine kinase into the incubation medium. Notably, when administered alongside the venom, AKH influenced the majority of these changes. AKH was the most effective in minimising damage to the ultrastructure of muscle cells and preventing the release of arginine kinase from muscles to the medium; however, in other parameters, the effect was modest or minimal. Given that honeybee venom often affects humans, understanding its actions and potential ways to reduce or eliminate them is valuable and could lead to the development of pharmacologically important compounds that may have clinical relevance.

• Keywords
• Adipokinetic hormone, Arginine kinase, Bee venom, Drosophila model, Immune responsible genes, Muscle structure,
• MeSH
• Central Nervous System drug effects   metabolism   MeSH
• Drosophila melanogaster drug effects   metabolism   MeSH
• Insect Hormones * pharmacology   metabolism   MeSH
• Pyrrolidonecarboxylic Acid * analogs & derivatives   pharmacology   metabolism   MeSH
• Oligopeptides * pharmacology   metabolism   MeSH
• Bee Venoms * toxicity   antagonists & inhibitors   MeSH
• Bees MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• adipokinetic hormone MeSH Browser
• Insect Hormones * MeSH
• Pyrrolidonecarboxylic Acid * MeSH
• Oligopeptides * MeSH
• Bee Venoms * MeSH

The impact of disruption of adipokinetic hormone (AKH) signaling was studied during aging in Drosophila in a sexually dimorphic manner. A mutant (Akh1) producing a non-functional AKH peptide was compared with isogenized wild-type controls (w1118), and Akh-rescue line where AKH was ectopically expressed in the mutant background (EE-Akh). Longevity, fecundity, and locomotor activity rhythms remained unaffected by lack of AKH signaling. While the strength of rhythms declined in general with age across all fly lines tested this was more so in case of Akh1 flies. Negative geotaxis was significantly impaired in Akh1 flies. Only young Akh1 flies of both sexes and old Akh1 females showed significantly higher body weight compared to age-matched iso-control flies (except in case of EE-Akh). Expression of genes involved in energy homeostasis and aging indicated that dTOR and Akt expression were elevated in Akh1 flies compared to other genotypes, whereas AMPK and dFoxO expression levels were significantly reduced. Multivariate analysis of the distribution of lipid species revealed a significant accumulation of specific diglyceride (DG) and triglyceride (TG) lipid species, irrespective of sex, attributable in part due to lack of AKH. Moreover, irrespective of lack of AKH, older flies of all genotypes accumulated TGs. Taken together, the results strongly suggest that disruption of AKH has very subtle effects on physiology, behavior and lipid status during aging.

• Keywords
• AKH signaling, adipokinetic hormone, aging, energy homeostasis, lipid status, senescence,
• Publication type
• Journal Article MeSH