The human gut microbiota: Metabolism and perspective in obesity

Abstract

The gut microbiota has been recognized as an important factor in the development of metabolic diseases such as obesity and is considered an endocrine organ involved in the maintenance of energy homeostasis and host immunity. Dysbiosis can change the functioning of the intestinal barrier and the gut-associated lymphoid tissues (GALT) by allowing the passage of structural components of bacteria, such as lipopolysaccharides (LPS), which activate inflammatory pathways that may contribute to the development of insulin resistance. Furthermore, intestinal dysbiosis can alter the production of gastrointestinal peptides related to satiety, resulting in an increased food intake. In obese people, this dysbiosis seems be related to increases of the phylum Firmicutes, the genus Clostridium, and the species Eubacterium rectale, Clostridium coccoides, Lactobacillus reuteri, Akkermansia muciniphila, Clostridium histolyticum, and Staphylococcus aureus.

Keywords: gut; gut microbiota; immune system; metabolism; obesity.

Figure 1.

Possible mechanisms that related the obesity and intestinal dysbiosis with the physiological changes that contributed to the maintenance of obesity. GALT: gut-associated lymphoid tissue; IgA: immunoglobulin A; LPS: lipopolysaccharide; NF-κB: nuclear factor kappa B; CLA: conjugated linoleic acids; PPAR: peroxisome proliferator-activated receptor; LPL: lipoprotein lipase; Angptl4: angiopoietin like protein 4; GLP-1: glucagon-like peptide 1; PYY: peptide YY.