High–glycemic index carbohydrate increases nuclear factor-κB activation in mononuclear cells of young, lean healthy subjects

Abstract

BackgroundHigh–glycemic index diets have been linked to greater risk of cardiovascular disease and type 2 diabetes. Postprandial glycemia within the normal range may promote oxidative stress and inflammatory processes underlying the development of disease. ObjectiveWe explored acute differences in the activation of the inflammatory marker nuclear factor-κB after consumption of 2 carbohydrate meals matched for macronutrient and micronutrient composition but differing in glycemic index. DesignAfter an overnight fast, 10 young, lean healthy subjects were fed in random order 3 meals providing 50 g of available carbohydrate as glucose, white bread, or pasta. Venous blood samples were collected at 0, 1, 2, and 3 h, and nuclear proteins were extracted from mononuclear cells. Changes in nuclear factor-κB–p65 proteins were detected by Western blotting. Acute changes in other markers of oxidative stress (nitrotyrosine and soluble intercellular adhesion molecule-1) were also assessed. ResultsThe maximum increase in nuclear factor-κB activation was similar after the bread meal [mean (±SEM) area under the curve: 69 ± 16% optical densityh] and the glucose challenge (75 ± 9% optical densityh), but was 3 times higher than after the pasta meal (23 ± 5% optical densityh) (P < 0.05). Similarly, changes in nitrotyrosine, but not soluble intercellular adhesion molecule-1, were higher after glucose and bread than after pasta (P = 0.01 at 2 h). ConclusionsThe findings suggest that high-normal physiologic increases in blood glucose after meals aggravate inflammatory processes in lean, young adults. This mechanism may help to explain relations between carbohydrates, glycemic index, and the risk of chronic disease.