The prevalence of obesity has increased dramatically in recent decades, so have the risks of associated medical conditions, such as type 2 diabete and cardiovascular disease, raising serious concerns for public health. Obesity is encouraged by current obesogenic environmental conditions that promote the intake of high-energy-dense foods and increased portion sizes. Cafeteria animal models provide a useful tool to study the metabolic syndrome in humans. Several animal studies and clinical trials suggest that marine bioactive oils supply may have potential effects on obesity and its associated features. Thus, the aim of this study was to evaluate the effects of krill oil enrichment in cafeteria-diet-overfed rats and their capacity to respond to acute changes on some antioxidant/ oxidant markers.

Eighteen aging male Wistar rats were divided into three groups of six each and were exposed for the ensuing 8 weeks to one of the diets : control group (C) which was submitted to standard chow (330kcal/100g), containing 24% of proteins, 5% of lipids and 70% of carbohydrates. Cafeteria standard group (CS) exposed to cafeteria diet (420kcal/100g) containing 30g of standard chow and 30g of sausage-dry cookies mixture, cheese, chips, chocolate, and peanuts in proportions of 2:2:2: 1:1:1. The last group received a cafeteria diet enriched in oral force-feeding krill oil 2% (KO-CS).

Despite modest differences in body weight, cafeteria-fed animals underwent an exacerbated body fat accumulation and increased metabolic risk. The substitution of standard chow diet by the cafeteria diet induced several disturbances in term of metabolic response to the radical attack in key tissues involved in antioxidant defense as demonstrated by the increase of TBARS, 8-OHdG DNA damages marker and isoprostanes levels in cafeteria-diet-fed rats. The serum TBARS, 8-OHdG and isoprostanes levels were significantly lowered by 45% and 25% respectively in the in the KO-CS group compared to CS group. Serum uric acid and albumin contents were decreased respectively by 36% and 18% in the krill oil enriched CS group as compared to cafeteria group.

A short period of exposure to a cafeteria diet in is enough to disturb the metabolic response to the radical attack in key tissues involved in antioxidant defense. The important antioxidant activity of KO could probably be due to its bioactive compounds (n-3 PUFA, phenolic compounds, alpha-tocopherol, manganese). Thus, its incorporation in a dietetic program can be strategically effective for the prevention/management, indeed improvement of free radical attack in obese subjects, which will prevent the obesity complications.