Intergenerational Impact of Parental Zinc Deficiency on Metabolic and Redox Outcomes in Drosophila melanogaster

TL;DR

Low zinc in parents affects their fruit fly offspring's metabolism and health, with stronger effects in females.

Contribution

Shows that parental zinc deficiency causes intergenerational metabolic and redox changes in Drosophila.

Findings

Offspring of zinc-deficient parents had higher body weight and zinc levels.

Female offspring showed greater sensitivity to parental zinc deficiency.

Altered gene expression in zinc transport and metabolic pathways was observed.

Abstract

Zinc is an important nutrient for our bodies, but many people do not get enough of it. This study looked at fruit flies (Drosophila) to see if low zinc levels in both parents could affect their babies’ health. We found that the offspring of zinc-deficient parents gained more weight and had higher zinc levels themselves. However, these offspring also had problems with how their bodies used sugar and fat, and their ability to fight off damage from the environment was reduced. Interestingly, the study suggests these effects were worse in female offspring. This research highlights the importance of zinc for overall health and suggests that low zinc levels in parents might have consequences for their children. Further studies on these connections can help us develop strategies to improve health for future generations.

Zinc deficiency is a common nutritional disorder with detrimental health consequences. Whether parental zinc deficiency induces intergenerational effects remains largely unknown. We investigated the effects of a combined maternal and paternal zinc deficiency on offspring’s metabolic outcomes and gene expression changes in Drosophila melanogaster. The parent flies were raised on zinc-deficient diets throughout development, and their progeny were assessed. Offspring from zinc-deprived parents exhibited a significant (p < 0.05) increase in body weight and whole-body zinc levels. They also displayed disrupted glucose metabolism, altered lipid homeostasis, and diminished activity of antioxidant enzymes. Gene expression analysis revealed significant (p < 0.05) alterations in zinc transport genes, with increases in mRNA levels of dZIP1 and dZnT1 for female and male offspring, respectively. Both sexes exhibited reduced dZnT35C mRNA levels and significant (p < 0.05) increases in the mRNA levels of DILP2 and proinflammatory markers, Eiger and UPD2. Overall, female offspring showed higher sensitivity to parental zinc deficiency. Our findings underscore zinc’s crucial role in maintaining health and the gender-specific responses to zinc deficiency. There is the need for further exploration of the underlying mechanisms behind these intergenerational effects.

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