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Title: Acute effects of dietary glycemic index on antioxidant capacity in nutrient-controlled feeding study

item BOTERO, DIEGO - Boston Children'S Hospital
item EBBELING, CARA - Boston Children'S Hospital
item BLUMBERG, JEFFREY - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item RIBAYA-MERCADO, JUDY - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item CREAGER, MARK - Brigham & Women'S Hospital
item SWAIN, JANIS - Brigham & Women'S Hospital
item FELDMAN, HENRY - Boston Children'S Hospital
item LUDWIG, DAVID - Boston Children'S Hospital

Submitted to: Obesity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/20/2009
Publication Date: 6/18/2009
Citation: Botero, D., Ebbeling, C.B., Blumberg, J.B., Ribaya-Mercado, J.D., Creager, M.A., Swain, J.F., Feldman, H.A., Ludwig, D.S. 2009. Acute effects of dietary glycemic index on antioxidant capacity in nutrient-controlled feeding study. Obesity. 17(9):1664-1670.

Interpretive Summary: Following a meal, there is an increase in glucose concentrations in the blood, an event that can be quantified by calculations for a "glycemic index" or GI. The GI has been associated with the risk for heart disease and diabetes in observational studies of large populations. Clinical trials also indicate that high-GI compared with low-GI diets may cause insulin resistance, promote inflammation, and increase levels of LDL ("bad") cholesterol. Oxidative stress may contribute to many of the effects of high-GI diets. We designed a clinical trial to examine the effects of dietary GI on antioxidant capacity, oxidative stress, and risk factors for cardiovascular disease and diabetes in 12 overweight and obese, healthy individuals. We hypothesized that compromised antioxidant capacity in response to high blood glucose after a meal would occur in people consuming a high-GI diet. Under fasting conditions, we found a measure of the total antioxidant capacity of plasma was significantly higher after 1 week on the low-GI vs. high-GI diet, a time before most traditional risk factors for heart disease and diabetes are usually detected. Thus, oxidative stress may mediate, at least in part, some of the effects of a high-GI diet on health.

Technical Abstract: Oxidative stress, caused by an imbalance between antioxidant capacity and reactive oxygen species, may be an early event in a metabolic cascade elicited by a high glycemic index (GI) diet, ultimately increasing the risk for cardiovascular disease and diabetes. We conducted a feeding study to evaluate the acute effects of low-GI compared with high-GI diets on oxidative stress and cardiovascular disease risk factors. The crossover study comprised two 10-day in-patient admissions to a clinical research center. For the admissions, 12 overweight or obese (BMI:27-45kg/m2) male subjects aged 18-35 years consumed low-GI or high GI-diets controlled for potentially confounding nutrients. On day 7, after an overnight fast and then during a 5-h postprandial period, we assessed total antioxidant capacity (total and perchloric acid (PCA) protein-precipitated plasma oxygen radical absorbance capacity (ORAC) assay) and oxidative stress status (urinary F2 alpha-isoprostanes (F2IP)). On day 10, we measured cardiovascular disease risk factors. Under fasting conditions, total antioxidant capacity was significantly higher during the low GI vs. high-GI diet based on total ORAC (11,736 +/- 668 vs. 10,381 +/-612 micro mol Trolox equivalents/l, P = 0.002) and PCA-ORAC (1,276 +/-96 vs. 1210 +/- 96 micro mol Trolox equivalents/I,P=0.02). Area under the postprandial response curve also differed significantly between the two diets for total ORAC and PCA-ORAC. No diet effects were observed for the other variables. Enhancement in plasma total antioxidant capacity occurs within 1 week on a low-GI diet, before changes in other risk factors, raising the possibility that this phenomenon may mediate, at least in part, the previously reported effects on GI health.