Abstract
Obesity caused by excessive fat accumulation in adipocytes is a growing global problem and is a major contributing risk factor for many chronic metabolic diseases. There is increasing evidence that oxidative stress plays a crucial role in both obesity progression and obesity-related complications. In recent years, Drosophila models of diet-induced obesity and associated pathologies have been successfully developed through manipulation of carbohydrate or fat concentrations in the food. Obese flies accumulate triacylglycerols in the fat body, an organ homologous to mammalian adipose tissue and exhibit metabolic and physiological complications including hyperglycemia, redox imbalance and shortened longevity; these are all similar to those observed in obese humans. In this review, we summarize current data on the mechanisms of oxidative stress induction in obesity, with emphasis on metabolic switches and the involvement of redox-responsive signaling pathways such as NF-κB and Nfr2. The recent achievements with D. melanogaster model suggest a complicated relationship between obesity, oxidative stress, and longevity but the Drosophila model offers probably the best opportunities to delve further into unraveling these interactions, particularly the roles of antioxidants and of Nrf2-regulated responses, in order to increase our understanding of the obese metabolic phenotype and test and develop anti-obesity pharmaceuticals.
