Inflammation, obesity and comorbidities: the role of diet

Abstract

The adipocyte metabolism has been shown to change during the fat enlargement process associated to obesity. Several procoagulant proteins such as plasminogen activator inhibitor type 1, tissue factor or factor VII and also inducible nitric oxide synthase show higher expression in adipose tissue of obese people in comparison to lean. This overexpression could explain at least a part of the atherogenic and cardiovascular risk associated with obesity. In addition to cytokine secretion, many other features have been observed to be common to adipocyte and monocyte/macrophage lines: for example, phagocytic and microbicidal activities, and possibly a cellular plasticity of adipose precursors. Overweight and obesity are associated with an increased risk of such metabolic abnormalities as dyslipidemia, hypertension or type 2 diabetes mellitus and cardiovascular diseases, common features of the metabolic syndrome. Initially, insulin resistance or hyperinsulinemia was suggested as the origin of these abnormalities. More recent studies indicate that adipokynes have an important role in obesity-associated metabolic complications, and suggest that chronically elevated local or systemic concentrations of adipokynes contribute to the development of complications associated with obesity and metabolic syndrome. Considering all the evidence relating to diet and inflammation, the best diet for protecting against the metabolic derangements associated with obesity and metabolic syndrome would be high in fibre-rich cereals, fruit, vegetables, fish, virgin olive oil and nuts; moderate in wine; and low in meat, processed meat foods and trans-fatty acids.