RESUMO
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Recent studies have shown that elevated concentrations of plasma lipopolysaccharide (LPS) constitute a metabolic mechanism enough for triggering insulin resistance, obesity and type 2 diabetes in animal models, and that high fat diets lead to increased plasma LPS concentrations through changes in the gut flora. We review here the LPS effects in metabolic processes in vitro. In humans, an altered innate immune system has also been associated with metabolic disorders such as insulin resistance, high endotoxemia markers (LBP, sCD14) and low LPS-neutralizing proteins (adiponectin, bactericidal permeability-increasing protein, a-defensins and lactoferrin). In fact, insulin resistance is well known to be associated with inflammation, with a decrease in innate immune efficiency and a reduction in the production of antimicrobial proteins. In this revision, we propose a new view according to which buffering efficiency of the innate (AU)
