Undernutrition-induced stunting-like phenotype in Drosophila melanogaster

Abstract

Stunting resulting from undernutrition is a significant global health challenge, particularly in developing countries, yet its underlying mechanisms and consequences remain inadequately understood. This study utilizes <i>Drosophila melanogaster</i> as an in vivo model to investigate the molecular basis of stunting. Due to the conserved nature of signaling pathways between <i>Drosophila</i> and vertebrates, this organism serves as an effective model for studying growth disorders. The aim of this study was to establish a <i>Drosophila</i> model exhibiting a stunting-like phenotype and to elucidate the molecular mechanisms underlying this condition. The stunting phenotype was induced through dietary manipulation, involving a standard nutrient-rich diet (100%) and treatment diets with reduced concentrations of sucrose, glucose, yeast, and cornmeal at 50%, 25%, and 12.5%. Phenotypic assessments included measurements of larval body size, fecundity, survival rates, and locomotor activity, alongside molecular analyses of gene expression related to metabolism, cell proliferation, and survival, using RT-qPCR. Results demonstrated that undernutrition profoundly affected <i>D. melanogaster</i>, causing growth retardation, reduced larval body size, diminished fecundity, and lower survival rates, though locomotor function remained unaffected. Molecular analysis revealed a significant decrease in the expression of the <i>totA</i> gene and notable increases in the expression of <i>dilp5</i>, <i>srl</i>, and <i>indy</i> genes, with no significant changes observed in the expression of the <i>pepck</i> gene. These findings indicate that undernutrition induces a stunting-like phenotype, likely driven by alterations in the expression of genes associated with metabolism, cell proliferation, and survival. Overall, this study establishes <i>D. melanogaster</i> as a valuable in vivo model for studying stunting-like phenotypes resulting from nutritional deficiencies and provides insights into the molecular pathways involved in growth impairment.

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