Inflammatory Response to a High-fat, Low-carbohydrate Weight Loss Diet: Effect of Antioxidants

The objective of this study was to test the hypothesis that the inflammatory response to a high‐fat, low‐carbohydrate weight loss diet (HF) we previously observed was due to oxidative stress. Nineteen overweight subjects (BMI > 27 kg/m2) were randomly assigned to either an antioxidant supplement...

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Veröffentlicht in:Obesity (Silver Spring, Md.) Md.), 2008-07, Vol.16 (7), p.1573-1578
Hauptverfasser: Peairs, Abigail T., Rankin, Janet W.
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Sprache:eng
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Zusammenfassung:The objective of this study was to test the hypothesis that the inflammatory response to a high‐fat, low‐carbohydrate weight loss diet (HF) we previously observed was due to oxidative stress. Nineteen overweight subjects (BMI > 27 kg/m2) were randomly assigned to either an antioxidant supplement (AS) (1 g vitamin C/800 IU vitamin E) or a placebo (P) group and provided with a HF for 7 days. Fasted pre‐ and post serum samples were measured for markers of inflammation (C‐reactive protein (CRP), interleukin‐6 (IL‐6), and monocyte chemoattractant protein‐1 (MCP‐1)), oxygen radical absorbance capacity (ORAC), and glucose, whereas urine was measured for oxidative stress (8‐epi‐prostaglandin‐F2α (8‐epi)). HF resulted in significant reductions in weight (−3.2%), glucose (−18.7%), and MCP‐1 (−15%) (all P < 0.01), with no difference between groups. There was a trend for a differential effect between groups for CRP as it decreased 32% in the AS group but increased 50% for P (P = 0.076). Inverse correlations were noted between initial values and changes in several inflammatory and oxidative stress markers, including CRP (r = −0.501), 8‐epi (r = −0.863), and ORAC (r = −0.546) (all P < 0.05). It was concluded that weight loss on a short‐term HF caused reduction of some but not all markers of inflammation. A role for oxidative stress in causing inflammation was not confirmed; however, longer term diet‐controlled studies are necessary to further explore the trend for a differential response in CRP with antioxidant supplementation.
ISSN:1930-7381
1930-739X
DOI:10.1038/oby.2008.252