Background
Gene-environment interactions play a crucial role in shaping the health of the offspring, with environmental factors like dietary zinc deficiency exerting significant impacts. Yet, the effect of parental zinc deficiency on the health of the offspring demands a holistic approach beyond solely examining maternal zinc status.
Aim
In this study, we investigated the physiological and molecular basis of both maternal and paternal zinc deficiency on offspring metabolic health, using the Drosophila melanogaster model.
Methods
Dietary zinc deficiency was induced in flies by incorporating TPEN (N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine) into their diet, starting from the egg stage through adulthood. Offspring were subsequently raised on standard diets. Following adulthood, parents and offspring were assessed for various parameters after seven days of exposure. Male and female flies (n = 10) were weighed and their locomotion was analysed. After being anaesthetized with ice, haemolymph was extracted and used to measure levels of glucose, trehalose, triglycerides, malondialdehyde, catalase activity, and total antioxidant capacity using commercially available kits. Finally, RNA was extracted, and quantitative real-time PCR (qPCR) was used to assess the mRNA expression of genes involved in zinc transport (dZIP1, dZnT1, dZIP71B, and dZnT53), glucose regulation (DILP2 and PEPCK), antioxidant defence (SOD1 and CAT), and inflammatory pathways (UPD2 and Eiger). Data were analysed using two-way ANOVA followed by Bonferroni multiple comparison post hoc test and expressed as mean ± standard deviation.
Results
While parental flies exhibited significantly reduced (p<0.05) body weight, both male and female offspring showed increased body weight. Moreover, the offspring manifested disruptions in glucose metabolism, lipid homeostasis, and antioxidant enzyme activity. Gene expression analysis revealed significant (p<0.05) alterations in zinc transport genes, with elevated dZIP1 mRNA levels in females and increased dZnT1 mRNA levels in males. Both sexes displayed reduced dZnT35C mRNA fold change. Additionally, DILP2 and the pro-inflammatory markers Eiger and UPD2 mRNA were upregulated.
Conclusion
This study reveals the lasting consequences of paternal zinc deficiency, impacting offspring health and highlighting the need to consider both parents when studying intergenerational health effects. Understanding these mechanisms could lead to preventative strategies against zinc deficiency-related metabolic disorders.
Keywords: Zinc deficiency, intergenerational, Drosophila melanogaster, metabolism, zinc transport