INVIVO GLUCOSE-METABOLISM IN OBESE AND TYPE-II DIABETIC SUBJECTS WITHOR WITHOUT HYPERTENSION

This study examined whether the presence of hypertension, an insulin-r esistant condition, exacerbates the defect in insulin action observed in obesity and type II diabetes mellitus. Glucose metabolism in the ba sal state and in response to insulin was quantitated by using the eugl ycemic insulin (20 mU . min-1 . m-2) clamp in combination with 3-[H-3] glucose infusion and indirect calorimetry in 20 obese nondiabetic subj ects (10 hypertensive and 10 normotensive), 26 type II diabetic subjec ts (13 hypertensive and 13 normotensive), and 11 normal nondiabetic su bjects. The two groups of obese subjects and the two groups of diabeti c subjects were matched for sex, age, race, body mass index, and fat d istribution. Both in the basal state and during insulin infusion, gluc ose disposal rates (total, oxidative, and nonoxidative) were similar i n obese subjects with or without hypertension. Compared with control s ubjects, both groups of obese subjects were markedly insulin resistant . Similarly, type II diabetic individuals, whether normotensive or hyp ertensive, were equally insulin resistant. The severity of insulin res istance was nearly identical in obese and diabetic groups. In diabetic subjects, the inhibitory effect of insulin on hepatic glucose output, lipolysis, and lipid oxidation was blunted compared with normal subje cts. In obese subjects the ability of insulin to inhibit lipolysis and lipid oxidation was impaired. However, hypertension did not alter the suppressive effects of insulin on hepatic glucose production, plasma free fatty acid levels, or lipid oxidation in either obese or type II diabetic subjects. These results indicate that hypertension does not c onfer a greater severity of insulin resistance than that already is pr esent in obesity and type II diabetes mellitus.