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Modulation of C-Reactive Protein, Tumor Necrosis Factor-α, and Adiponectin by Diet, Exercise, and Weight Loss

Author:
Puglisi, Michael J., Fernandez, Maria Luz
Source:
Journal of nutrition 2008 v.138 no.12 pp. 2293-2296
ISSN:
0022-3166
Subject:
diet-related diseases, diet, exercise, C-reactive protein, atherosclerosis, humans, adiponectin, inflammation, tumor necrosis factor-alpha, chronic diseases, weight loss, antioxidants
Abstract:
Chronic disease has been strongly correlated with inflammation resulting from the body's release of inflammatory cytokines as a result of injury or infection. Specific interventions promoting weight loss, exercise, or intake of antioxidants have been used by several investigators in an effort to decrease inflammatory cytokines. C-reactive protein (CRP) is produced by the liver and its role in the development of inflammation has been well established. However, the strong association between CRP and risk for heart disease is a more recent discovery. During the inflammation process, the transcriptional activity of nuclear factor κB leads to the increased production of inflammatory cytokines associated with atherosclerosis, including tumor necrosis factor-α (TNFα). Increased concentrations of TNFα have been reported in obese patients; thus, weight loss is considered a key intervention to reduce the concentrations of this cytokine. In contrast to CRP and TNFα, adiponectin increases during weight loss and insulin sensitivity. Additionally, lower concentrations of this cytokine have been reported in cardiovascular disease and type-2 diabetes. Recent epidemiological studies and clinical interventions have reported contradictory findings related to dietary or exercise interventions and the resulting alterations in plasma cytokines. Part of the discrepancies may be due to the population studied, the time of the treatment, and the lack of weight loss in some studies. Although it is clear from the literature that these cytokines play a major role in the development of chronic disease, the best strategy to favorably alter the inflammatory response is still debatable.
Agid:
1455093