Abstract
Whether PUFA diets affect inflammatory mediators in central and peripheral sites is not clear. We investigated the effect of high-fat PUFA diets on the expression of proteins involved in inflammatory pathways in hypothalamus, muscle, and liver. Male rats were fed for 2 months with either chow or high-fat diets enriched with either soy (n-6 PUFAs) or fish oil (n-3 PUFAs). The fish group had normal body weight, low serum NEFA, reduced hypothalamic levels of TNF-α, IL-6, and TRAF6, and increased levels of IL-10 receptor. In contrast, the soy group had increased body weight and hypothalamic levels of TRAF6 and NFκBp65. In muscle, the fish diet reduced TNF-α and IL-6 levels. Both PUFA diets increased muscle IL-10 levels and reduced liver TNF-α and IL-6 levels. The data showed that the high-fat soy diet induced activation of the hypothalamic NFκB inflammatory pathway, a feature predisposing to feeding and energy expenditure disturbances associated with the development of obesity. On the other hand, the high-fat fish diet improved the central and the peripheral inflammatory profile via reduction of intracellular inflammatory mediators, suggesting a protection against obesity.
Highlights
Obesity is known to present an inflammatory process of low grade, with elevated levels of cytokines such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β), contributing to the pathogenesis of important disturbances of the obese condition, as insulin resistance and metabolic defects
Its interactions with several proteins leads to phosphorylation of the inhibitory factor IκB, which is targeted for proteosomal degradation, releasing nuclear factor κB (NFκB), whose p65 subunit undergoes phosphorylation and translocates to the nucleus, where it binds to its target genes to produce proinflammatory cytokines [5]
The hypothalamus is a key regulator of energy homeostasis, through the production of orexigenic and anorexigenic neuropeptides targeted by the peripheral hormones leptin and insulin, which exert a pivotal control food intake and energy expenditure
Summary
Obesity is known to present an inflammatory process of low grade, with elevated levels of cytokines such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β), contributing to the pathogenesis of important disturbances of the obese condition, as insulin resistance and metabolic defects. This inflammatory state has been described to induce elevated signaling through the toll-like receptors TLR2 and TLR4, with activation of the nuclear factor κB (NFκB) pathway in muscle, liver, and adipose tissue [1,2,3,4]. We have shown that the disruption of these hypothalamic mechanisms, including insulin, leptin, and serotonin systems, is associated with obesity [11,12,13,14,15,16]
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