Dysbiotic Gut Bacteria in Obesity: An Overview of the Metabolic Mechanisms and Therapeutic Perspectives of Next-Generation Probiotics

Jonathan Breton, Marie Galmiche, Pierre Déchelotte, Jonathan Breton, Marie Galmiche, Pierre Déchelotte

Abstract

Obesity, a worldwide health concern with a constantly rising prevalence, is a multifactorial chronic disease associated with a wide range of physiological disruptions, including energy imbalance, central appetite and food reward dysregulation, and hormonal alterations and gut dysbiosis. The gut microbiome is a well-recognized factor in the pathophysiology of obesity, and its influence on host physiology has been extensively investigated over the last decade. This review highlights the mechanisms by which gut dysbiosis can contribute to the pathophysiology of obesity. In particular, we discuss gut microbiota's contribution to host energy homeostatic changes, low-grade inflammation, and regulation of fat deposition and bile acid metabolism via bacterial metabolites, such as short-chain fatty acids, and bacterial components, such as lipopolysaccharides, among others. Finally, therapeutic strategies based on next-generation probiotics aiming to re-shape the intestinal microbiota and reverse metabolic alterations associated with obesity are described.

Keywords: gut microbiota; intestinal dysbiosis; metabolic syndrome; next-generation probiotics; obesity.

Conflict of interest statement

P.D. is a shareholder and consultant for TargEDys SA. The other authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Gut microbiota’s contribution to obesity development. TLR: Toll-Like Receptor; GPR: G-protein coupled receptor; FXR: Farnesoid X Receptor; TGR5: Takeda G protein-coupled receptor 5; SCFAs: Short-Chain Fatty Acids; LPS: lipopolysaccharides; PPAR: Peroxisome proliferator-activated receptors; FIAF: Fasting-induced adipose factor; ANGPTL; angiopoietin-like protein; BA: Bile Acid, EE, Entero-endocrine cells; CCK: Cholecystokinin; PYY: peptide tyrosine tyrosine; GLP-1: Glucagon-like peptide 1; AMPK: AMP-activated protein kinase, NF-κB: Nuclear factor-kappa B.

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Source: PubMed

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구독하다