GLUCOSE-METABOLISM IN ABDOMINALLY OBESE HYPERTENSIVE AND NORMOTENSIVESUBJECTS

To determine whether the combination of obesity and hypertension resul ts in additive defects in oxidative and nonoxidative glucose metabolis m and the association of these changes with altered hemodynamic action s of insulin, we studied 11 abdominally obese hypertensive, 6 abdomina lly obese normotensive, and 7 lean normotensive nondiabetic subjects. Endogenous glucose production and glucose metabolized were calculated from a euglycemic clamp at 72 and 287 pmol insulin/m(2)-per minute. Gl ucose metabolized divided by insulin was lower at 72 pmol/m(2) per min ute in both obese groups than in lean normotensive subjects, at 148+/- 14, 144+/-33, and 373+/-69 (mu mol/m(2) per minute)/(pmol/L), respecti vely (P<.01). Similar results were obtained during the higher insulin dose. Nonoxidative and oxidative glucose disposals by indirect calorim etry were lower in both abdominally obese groups (P<.05). Hepatic gluc ose production was completely suppressed in lean subjects at the lower insulin dose and in all three groups at the higher insulin dose. Hemo dynamic responses during the clamp were not significantly different am ong the three groups. Abdominal obesity is associated with defects in insulin-regulated oxidative and nonoxidative glucose disposal as well as in insulin suppression of hepatic glucose production. Mild hyperten sion does not exacerbate these defects. Whereas the global impairment in glucose metabolism suggests the presence of an early defect or defe cts, including reduced tissue perfusion, systemic and regional hemodyn amic responses to insulin were not altered. These findings do not supp ort a direct role for insulin resistance in the pathogenesis of the hy pertension associated with abdominal obesity.