Obesity and insulin resistance are frequently associated with chronic low grade inflammation.  Animal Evidence for this has largely come from high fat fed mouse models however the development of inflammation and obesity in rats on similar diets is less common.  The more palatable “cafeteria-style” diet appears to be more effective at inducing obesity in rats compared to standard high fat diets.  Therefore we chose to explore the relationship between inflammation and insulin resistance in the cafeteria diet model.  Male Sprague Dawley rats were fed either a high caloric cafeteria-style diet consisting of popular snack food items, or a control diet (5% fat wt/wt) for 4 weeks.  After the 4 week dietary intervention, rats underwent hyperinsulinemic euglycaemic clamps (10mU/min/kg).  The cafeteria diet was successful in inducing obesity with body weight (292±5 vs 346±6 g) and epididymal fat pad weight (0.96±0.1 vs 2.16±0.1 g) significantly different between rats fed the cafeteria diet and control animals.  Glucose infusion rate during the clamp was found to be impaired in the cafeteria diet-fed rats compared to controls (26±0.6 vs 23±1.2 mg.min-1.kg-1) indicating insulin resistance.  Despite being associated with obesity and insulin resistance, at 4 weeks the cafeteria diet-fed rats showed no signs of inflammation in skeletal muscle or adipose tissue (Table 1).  These findings suggest that inflammation is not always present in obesity, and is not necessary for the development of insulin resistance.  Therapeutic approaches based solely on targeting inflammation mediated effects thus may not be universally applicable for the treatment of insulin resistance and diabetes.