To clarify on a cellular basis the mechanism of the diabetogenic effect of the westernized diet, insulin binding, insulin stimulated 3-o-methylglucose uptake and glucose oxidation were studied in isolated adipocytes from rats fed experimental diets : low fat-no sugar diet (energy ratio of 10% fat, 70% starch, a model of the traditional Japanese diet), high fat-high sugar diet (40% fat, 20% starch, 20% sugar, a model of the westernized diet), low fat-high sugar diet (10% fat, 50% starch, 20% sugar) and high fat-no sugar diet (40% fat, 40% starch). In high fat-high sugar diet rats, epididymal fat and mean fat cell size were significantly greater than in low fat-no sugar diet rats. There was no significant difference in insulin binding and insulin stimulated 3-o-methylglucose uptake between high fat-high sugar diet rats and low fat-no sugar diet rats. However, insulin stimulated glucose oxidation was markedly lower in high fat-high sugar diet rats. Therefore, it is suggested that the high fat-high sugar diet induced a post-receptor defect but did not influence receptor binding in rat adipocytes. In high fat-no sugar diet rats, a similar post-receptor defect was found, but in low fat-high sugar diet rats, insulin binding and post-receptor insulin action were unchanged. In conclusion, the high fat-high sugar diet may produce diabetogenic effects through reduced insulin action due to a postreceptor defect.