Probiotics and Gut Microbiota in Obesity: Myths and Realities of a New Health Revolution

Xavier Eugenio León Aguilera, Alexander Manzano, Daniela Pirela, Valmore Bermúdez, Xavier Eugenio León Aguilera, Alexander Manzano, Daniela Pirela, Valmore Bermúdez

Abstract

Obesity and its comorbidities are humans' most prevalent cardio-metabolic diseases worldwide. Recent evidence has shown that chronic low-grade inflammation is a common feature in all highly prevalent chronic degenerative diseases. In this sense, the gut microbiota is a complete ecosystem involved in different processes like vitamin synthesis, metabolism regulation, and both appetite and immune system control. Thus, dysbiosis has been recognised as one of the many factors associated with obesity due to a predominance of Firmicutes, a decrease in Bifidobacterium in the gut, and a consequent short-chain fatty acids (SCFA) synthesis reduction leading to a reduction in incretins action and intestinal permeability increase. In this context, bacteria, bacterial endotoxins, and toxic bacterial by-products are translocated to the bloodstream, leading to systemic inflammation. This review focuses on gut microbiota composition and its role in obesity, as well as probiotics and prebiotics benefits in obesity.

Keywords: gut microbiota; obesity; prebiotics; probiotics; short chain fatty acids.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Gut microbiota composition: Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria are the four “standard” Phyla in our gut intestinal microbiota. Each phylum comprises bacteria with diverse structures, metabolism, and functions.
Figure 2
Figure 2
Main effects of short-chain fatty acids (SCFA) on microbiota and epithelium barrier. SCFA protect the intestinal barrier by lowering the levels of TNFα and interleukin (IL)-6, activating the G-protein coupled receptors (GPCR) to participate in PParα expression increase and the intestinal-mediated inflammatory and immune response by suppressing histone deacetylase (HDAC) and downregulating the expression of pro-inflammatory cytokines. Additionally, SCFA upregulates the gene expression of mucin family genes (MUC1–4) in the intestine, and the protons generated by SCFA dissociation produce an osmotic pressure imbalance in the bacteria. Furthermore, SCFA inhibits bacterial multiplication by interfering with DNA and protein synthesis.
Figure 3
Figure 3
Dietary fibre and its effects on human metabolism and gut microbiota.

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Source: PubMed

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