Behavioural treatments for chronic systemic inflammation: effects of dietary weight loss and exercise training. CMAJ

Sticht Center on Aging, Section on Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Canadian Medical Association Journal (Impact Factor: 5.96). 05/2005; 172(9):1199-209. DOI: 10.1503/cmaj.1040769
Source: PubMed


Persistent low-grade inflammation, as indicated by higher circulating levels of inflammatory mediators such as C-reactive protein, interleukin-6 and tumour necrosis factor-alpha, is a strong risk factor for several chronic diseases. There are data indicating that decreasing energy intake and increasing physical activity may be effective therapies for reducing overall inflammation. Evidence is strong that circulating levels of inflammatory markers are elevated with total and abdominal obesity, possibly owing to a higher secretion rate of cytokines by adipose tissue in obese people. Moreover, very-low-energy dietary weight loss reduces both circulating markers of inflammation and adipose-tissue cytokine production. Data from several large population-based cohorts show an inverse association between markers of systemic inflammation and physical activity or fitness status; small-scale intervention studies support that exercise training diminishes inflammation. Dietary weight loss plus exercise is likely more effective than weight reduction alone in reducing inflammation. To date, data from randomized, controlled trails designed to definitively test the effects of weight loss or exercise training, or both, on inflammation are limited. Future studies are required to define the amount of weight loss needed for clinically meaningful reductions of inflammation; in addition, fully powered and controlled studies are necessary to clarify the effect of exercise training on chronic, systemic inflammation.

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    • "Several studies have shown that obese people and/or patients with T2D have increased serum levels of IL-6 (Pradhan et al., 2001). Conversely, IL-6 levels decrease when obese people lose weight (Nicklas et al., 2005). In the last 20 years it has become clear that obesity is associated with low grade chronic inflammationHotamisligil, 2006). "

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    • "The adipose tissue, as an active endocrine organ, activates pro-inflammatory serine kinase cascade signaling pathways which promote the secretion of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) [6] [7] [8]. IL-6 and TNF-α in turn are both stimulators of C-Reactive Protein (CRP) release from hepatocytes [8] [9]. Therefore, higher levels of highsensitivity (hs)CRP, IL-6 and TNF-α indicate an inflammatory state in obese subjects [8,10–12], which plays an important role in atherosclerotic processes [13]. "
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    ABSTRACT: Obesity is associated with inflammation and weight reduction has been shown to influence the inflammatory process. Besides classic inflammatory markers, oxidized polyunsaturated fatty acid (PUFA) metabolites (oxylipins) are potent mediators of inflammation. Little is known about endogenous levels of oxylipins, e.g. hydroxy, epoxy and dihydroxy FA in obese subjects with persistent low-grade inflammation. We aimed to evaluate levels of inflammatory markers and blood oxylipins in obese subjects before and after weight reduction.
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    • "Increased production of anti-inflammatory mediators by adipocytes and decreased hepatic production of fibrinogen and other proinflammatory mediators are other consequences of exercise-induced weight reduction. Weight loss also influences the immune system by reducing the number of mononuclear cells in the circulation; these are important sources of proinflammatory cytokines [122]. The effect of exercise training on reducing the expression of TNF-α in white adipose tissue has been shown in several animal studies, as well [123–125]. "
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    ABSTRACT: The lack of adequate physical activity and obesity created a worldwide pandemic. Obesity is characterized by the deposition of adipose tissue in various parts of the body; it is now evident that adipose tissue also acts as an endocrine organ capable of secreting many cytokines that are though to be involved in the pathophysiology of obesity, insulin resistance, and metabolic syndrome. Adipokines, or adipose tissue-derived proteins, play a pivotal role in this scenario. Increased secretion of proinflammatory adipokines leads to a chronic inflammatory state that is accompanied by insulin resistance and glucose intolerance. Lifestyle change in terms of increased physical activity and exercise is the best nonpharmacological treatment for obesity since these can reduce insulin resistance, counteract the inflammatory state, and improve the lipid profile. There is growing evidence that exercise exerts its beneficial effects partly through alterations in the adipokine profile; that is, exercise increases secretion of anti-inflammatory adipokines and reduces proinflammatory cytokines. In this paper we briefly describe the pathophysiologic role of four important adipokines (adiponectin, leptin, TNF- α, and IL-6) in the metabolic syndrome and review some of the clinical trials that monitored these adipokines as a clinical outcome before and after exercise.
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