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J Clin Endocrinol Metab. 2007 Nov;92(11):4476-9. Epub 2007 Sep 4.

Prolonged reactive oxygen species generation and nuclear factor-kappaB activation after a high-fat, high-carbohydrate meal in the obese.

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  • 1Division of Endocrinology, Diabetes, and Metabolism, State University of New York at Buffalo and Kaleida Health, Buffalo, New York 14209, USA.

Abstract

BACKGROUND:

Because obesity is associated with chronic oxidative and inflammatory stress, and high-fat, high-carbohydrate meals induce significant oxidative and inflammatory stress in normal subjects, we have now hypothesized that the intake of a high-fat, high-carbohydrate meal would result in a greater and more prolonged oxidative and inflammatory stress in the obese than in normal subjects.

METHODS:

Ten normal-weight and eight obese subjects were given a high-fat, high-carbohydrate meal after an overnight fast. Blood samples were collected at baseline and hourly following the meal for 3 h.

RESULTS:

Reactive oxygen species generation by mononuclear cells increased significantly by 2 h in both groups but continued to increase significantly at 3 h in the obese subjects, whereas in normal subjects it returned to baseline. Levels of p47(phox) increased significantly (by 81 +/- 26%) at 3 h in obese individuals (P < 0.05), whereas there was no significant change in p47(phox) in normal subjects. Nuclear factor-kappaB DNA binding in mononuclear cells increased significantly (by 48 +/- 58%, P < 0.036) at 2 h but not at 3 h in normal subjects, whereas in the obese, nuclear factor-kappaB increased significantly at both 2 and 3 h (by 36 +/- 57 and 42 +/- 63%, respectively, P < 0.004). Matrix metalloproteinase-9 concentrations were significantly higher in the obese at baseline (580 +/- 103.9 vs. 373 +/- 30.03 ng/ml, P < 0.05) and increased to significantly greater concentrations after the meal than in the lean subjects.

CONCLUSIONS:

High-fat, high-carbohydrate meals induced a significantly more prolonged and greater oxidative and inflammatory stress in the obese. This may contribute to the increased atherogenic risk in obesity.

PMID:
17785362
DOI:
10.1210/jc.2007-0778
[PubMed - indexed for MEDLINE]
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