A FRUCTOSE-RICH DIET DECREASES INSULIN-STIMULATED GLUCOSE INCORPORATION INTO LIPIDS BUT NOT GLUCOSE-TRANSPORT IN ADIPOCYTES OF NORMAL AND DIABETIC RATS

To study the cellular mechanisms underlying fructose-induced insulin r esistance in rats, the effects of fructose feeding on insulin-stimulat ed glucose transport, oxidation and incorporation into lipids in epidi dymal adipocytes were evaluated in 27 normal and 27 noninsulin-depende nt diabetic male Sprague-Dawley rats. Diabetes was induced by streptoz otocin injection 2 d after birth. At 5 wk of age, both normal and diab etic rats were fed a diet containing 62% carbohydrate as fructose, dex trose or cornstarch. Fructose feeding for 6 wk induced glucose intoler ance in normal rats (P < 0.05) and aggravated that of diabetic rats (P < 0.05). Plasma triacylglycerol concentration was higher in fructose- fed than in starch-feel or dextrose-fed rats (P < 0.05). Adipocytes of fructose-fed rats had significantly lower maximum insulin-stimulated glucose incorporation into total lipids than those of rats fed starch, and tended (P = 0.22) to have lower production of CO2 from glucose th an adipocytes of the other dietary groups. Glucose transport in adipoc ytes of dextrose-, starch- and fructose-fed rats did not differ. We co nclude that in both normal and diabetic rats, a chronic fructose-rich diet induced hypertriacylglycerolemia, glucose intolerance and insulin resistance of adipocytes.