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Gut Microbiota Modulation and Its Relationship With Obesity Using Prebiotic Fibers and Probiotics: A Review


Gut Microbiota Modulation and Its Relationship With Obesity Using Prebiotic Fibers and Probiotics: A Review

Dinesh K Dahiya et al. Front Microbiol.


In the present world scenario, obesity has almost attained the level of a pandemic and is progressing at a rapid rate. This disease is the mother of all other metabolic disorders, which apart from placing an added financial burden on the concerned patient also has a negative impact on his/her well-being and health in the society. Among the various plausible factors for the development of obesity, the role of gut microbiota is very crucial. In general, the gut of an individual is inhabited by trillions of microbes that play a significant role in host energy homeostasis by their symbiotic interactions. Dysbiosis in gut microbiota causes disequilibrium in energy homeostasis that ultimately leads to obesity. Numerous mechanisms have been reported by which gut microbiota induces obesity in experimental models. However, which microbial community is directly linked to obesity is still unknown due to the complex nature of gut microbiota. Prebiotics and probiotics are the safer and effective dietary substances available, which can therapeutically alter the gut microbiota of the host. In this review, an effort was made to discuss the current mechanisms through which gut microbiota interacts with host energy metabolism in the context of obesity. Further, the therapeutic approaches (prebiotics/probiotics) that helped in positively altering the gut microbiota were discussed by taking experimental evidence from animal and human studies. In the closing statement, the challenges and future tasks within the field were discussed.

Keywords: gut microbiota; nanotechnology; obesity; prebiotic; probiotics.


Possible mechanisms associated with the intake of high fat diet and obesity. (A) High fat diet causes alteration in intestinal microbiota from low to high Firmicutes and high to low Bifidobacterium. (B) Low expression of AMPK leads to decreased fatty acid oxidation. (C) FIAF expression causes activation of LPL that leads to TGs accumulation. (D) Low GLP-1 leads to increased insulin resistance and decreased bile acid secretion from liver. (E) Decreased PYY causes low satiety in obese host. (F) Increased lipogenesis via upregulated Acc1 and Fas enzymes. (G) Activation of endo cannabinoid loop via release of LPS due to damages intestinal epithelium. (H) Modulation of intestinal immune response via TLR-5 downstream signaling. (I) Systemic inflammation caused by inflammatory cytokines and bacterial LPS.

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