Abstract
Obesity is associated with the presence of chronic subclinical inflammation due to excessive secretion of proinflammatory and reduced secretion of anti-inflammatory factors in adipose tissue. Low grade inflammation contributes to the development of metabolic complications, especially type 2 diabetes and dyslipidemia, as well as to an increased risk of cardiovascular disorders and cancer.
Gastrointestinal tract dysfunction may also contribute to obesity-associated subclinical inflammation. This dysfunction is characterized by increased permeability of gastrointestinal tract for bacterial toxins with excessive penetration of endotoxin into circulation and changes of the composition of the gut microbiota with potentially important metabolic consequences.
The aim of this paper is to summarize current knowledge of new ethiopathogenetic mechanisms linking obesity and subclinical inflammation focusing on the relationship between the intestinal microbiota, low grade inflammation and metabolic complications.