高脂肪食および高砂糖食のラット脂肪細胞におけるインスリン結合およびインスリン作用におよぼす影響

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.