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Obesity represents a major public health problem, as it leads to metabolic disorders involved in the development of type 2 diabetes, fatty liver diseases, cardiovascular diseases and cancer (1). The Weste lifestyle, including over-feeding of highly refined diets and sedentary behavior, is associated with systemic low-grade inflammation, responsible for chronic degenerative disease. Moreover, animal and human data have demonstrated the impact of high-fat diet feeding on the onset of metabolic endotoxemia. This latter, being characterized by increase blood lipopolysaccharide (LPS) levels, triggers low-grade inflammation and contributes to the development of obesity. The gut microbiota are a candidate sources of plasma LPS. Indeed, LPS is a major component of the outer membrane in Gram-negative bacteria and its plasma levels are correlated with changes in intestinal microbiota where the Gram-negative to Gram-positive ratio is increased by high fat feeding (1). Not surprising that in humans, obesity is characterized by dysbiosis, i.e. imbalances in the composition and function of the intestinal microbes. Currently, many studies are being conducted to assess the contribution of intestinal microflora metabolites [mainly short-chain fatty acids (SCFAs)] to the organism’s homeostasis. Dietary fibers have been promoted for their health benefits and high-fiber intake has been reported as beneficial in numerous chronic diseases (2). However, we have to keep in mind that consumption of dietary fiber significantly alters the composition of the gut microbiota. For instance, addition of fibers to the diet increases the abundance of butyrate-producing bacteria Roseburia species and Eubacterium rectale, whereas a low-fiber diet is associated to a major decrease in this group, with Faecalibacterium prausnitzii becoming the main