title: Inflammatory response to a high-fat, low-carbohydrate weight loss diet: effect of antioxidants.
abstract: 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/m(2)) 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-F(2alpha) (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.
authors.affiliation: Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, Virginia, USA. aturpyn@vt.edu
authors.forename: Abigail T
authors.initials: AT
authors.lastname: Peairs
authors.forename: Janet W
authors.initials: JW
authors.lastname: Rankin
mesh_terms: D000975:Antioxidants / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000627:therapeutic use*; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000187:drug effects; D002097:C-Reactive Protein / Q000378:metabolism; D018932:Chemokine CCL2 / Q000097:blood; D050528:Diet, Carbohydrate-Restricted / Q000009:adverse effects*; D004041:Dietary Fats / Q000008:administration & dosage / Q000009:adverse effects*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D004338:Drug Combinations; D005260:Female; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009765:Obesity / Q000178:diet therapy* / Q000188:drug therapy* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000097:blood; D013997:Time Factors; D016896:Treatment Outcome; D014810:Vitamin E / Q000627:therapeutic use; D015431:Weight Loss
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D001786:Blood Glucose; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D004041:Dietary Fats; D004338:Drug Combinations; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D017382:Reactive Oxygen Species; D014810:Vitamin E; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D015237:Dinoprost; D001205:Ascorbic Acid