DECREASED ADIPOSITY RESULTING FROM REDUCED FOOD INTAKE LIKELY CONTRIBUTES TO THE AMELIORATION OF GENOTOXIC...

Obesity is defined as the excessive accumulation of fat that can lead to the development of several diseases, such as type 2 diabetes and cardiovascular diseases. Dietary studies using animal models are essential to elucidate the mechanisms involved in obesity development. Diet-induced obesity models, including the cafeteria diet (CAF), have been employed to study obesity in rodents. Currently, research efforts have focused on treatment strategies for the metabolic dysfunctions caused by obesity. Omega-3 (O3) plays a crucial role in body development throughout life; therefore, this study aimed to evaluate the effect of O3 supplementation on biochemical and genotoxic parameters in mice that were fed a cafeteria diet. Forty-eight mice were divided into six groups (n=8/group): Standard Diet (SD); SD with O3 supplementation; CAF; CAF with O3 supplementation; CAF switched to SD; and CAF switched to SD with O3 supplementation. Animals were fed either a cafeteria or standard diet for 16 weeks and monitored for mass changes. O3 supplementation by gavage or diet switch began after the initial 16 weeks and lasted 4 weeks. At week 20, the mass was assessed again, and blood samples were collected for biochemical analyses and insulin tolerance tests. Following euthanasia, genotoxic analyses were performed. The present study demonstrated that the CAF diet led to increased food and energy intake, body mass, adiposity index, fasting blood glucose levels, insulin resistance, and genomic instability in mice. O3 supplementation partially attenuated these effects by reducing food intake, body weight, adiposity index, fasting blood glucose levels and DNA damage. The results of this study suggest that the observed improvements in metabolic and genotoxic parameters are primarily driven by reductions in energy intake and adiposity, with O3 supplementation being associated with reduced food intake under cafeteria diet conditions, highlighting its contribution to the modulation of obesity-related metabolic and genotoxic alterations.