Anthocyanins rescue Macrophage infiltration in a Drosophila model of obesity

For years, scientific research has availed itself of the opportunity of using animal models to understand the cellular and molecular mechanisms that regulate several human diseases. In this thesis, I showed the great importance to employ Drosophila melanogaster as model organism for the study of chronic diseases. Drosophila is considered an excellent and innovative model thanks to its peculiar characteristics such as low cost, small genome size, short generation time. About 75% of human disease-causing genes have functional homologs in Drosophila; furthermore, the fruit fly shows extreme genetic flexibility and a number of genetic systems has been developed to answer specific biological questions, such as the UAS-GAL4 binary system that allows the expression of target genes in a tissue-specific manner. For all these reasons, Drosophila can be used for the study of different metabolic diseases among which obesity. In particular, in our laboratory we created a new Drosophila model of obesity that shows similar characteristics as those present in obese people, promoting an Adipose Tissue Macrophages infiltration (ATM) phenotype. Using this new model of obesity, I tried to understand the role of important compounds like Flavonoids and Anthocyanins, both considered anti-inflammatory and antioxidant agents, which regular consumption reduces the risk to develop metabolic disorders. Anthocyanins represent the major red, purple, and blu pigment in many plants and fruits. I have discovered that Anthocyanins are able to rescue the ATM phenotype by reducing the Drosophila hemocytes (similar to human macrophages) migration in the larval fat body, which carries out human adipose tissue and liver functions. Anthocyanins also show potential health benefits by reducing ROS levels, thus acting as antioxidant agents. This antioxidant activity may be due to the capacity to modulate the expression of some redox regulators like Glutathione-S-Transferase (GST) and the Nuclear factor erythroid 2-Related Factor 2 (NRF2).