Publications

Abstract

BACKGROUND: Arterial stiffness, specifically augmentation index (AIx), is an independent predictor of cardiovascular risk. Previous studies suggest that insulin infusion decreases AIx and that this response is attenuated in insulin resistance. Whether physiological postprandial insulinemia similarly affects AIx measurements, and whether insulin resistance modifies this response, has not been studied. METHODS: Seven relatively insulin-resistant and seven insulin-sensitive postmenopausal women received low-carbohydrate and high-carbohydrate high-fat meals on separate days. Glucose and insulin levels were measured for 360-min following meal consumption. AIx was measured by radial artery applanation tonometry at regular intervals postprandially. RESULTS: Postprandial increases in glucose and insulin were greater following the high-carbohydrate high-fat meal in both insulin-sensitive and insulin-resistant subjects. AIx decreased in both groups following both meals. In insulin-sensitive subjects, the postprandial reduction (incremental area above the curve) in AIx was greater following the high-carbohydrate vs. low-carbohydrate high-fat meal (-6821+/-1089 vs. -3797+/-1171% x min, respectively, P=0.009). In contrast, in insulin-resistant subjects, postprandial AIx responses were similar following the meals, suggesting that insulin resistance is associated with impaired postprandial arterial relaxation. CONCLUSIONS: This study demonstrates that the carbohydrate content of a meal, and, hence, the magnitude of the postprandial glucose and insulin responses it elicits, are important determinants of postprandial AIx measurements. The further observation that insulin resistance modified this effect raises the possibility that this phenomenon is a contributor to increased cardiovascular risk in insulin resistance. The results indicate that future studies of AIx need to control for the effects of these potentially confounding variables and that measurement of AIx should be standardized with respect to meals.