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Review
. 2024 Spring;15(2):215-227.
doi: 10.22088/cjim.15.2.215.

Novel therapeutic strategy for obesity through the gut microbiota-brain axis: A review article

Romina Kardan  1   2 , Jaber Hemmati  3   4   2 , Mohsen Nazari  3   4 , Amjad Ahmadi  3   4 , Babak Asghari  4 , Mehdi Azizi  5 , Mansoor Khaledi  6 , Mohammad Reza Arabestani  4   7
Affiliations
Review

Novel therapeutic strategy for obesity through the gut microbiota-brain axis: A review article

Romina Kardan et al. Caspian J Intern Med. 2024 Spring.

Abstract

Background: The interaction between commensal bacteria and the host is essential for health and the gut microbiota-brain axis plays a vital role in this regard. Obesity as a medical problem not only affect the health of the individuals, but also the economic and social aspects of communities. The presence of any dysbiosis in the composition of the gut microbiota disrupts in the gut microbiota-brain axis, which in turn leads to an increase in appetite and then obesity. Because common treatments for obesity have several drawbacks, the use of microbiota-based therapy in addition to treatment and prevention of obesity can have other numerous benefits for the individual. In this review, we intend to investigate the relationship between obesity and the gut microbiota-brain axis as well as novel treatment strategies based on this axis with an emphasis on gut microbiota.

Keywords: Fecal Microbiota transplantation; Gut microbiota; Gut–brain axis; Obesity; Prebiotic; Probiotic.

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Conflict of interest statement

This study does not include any conflict of interest for the authors.

Figures

Figure 2
Figure 2
The microbiota and gut-brain axis. The communication between the brain and the gut takes place through different pathways as well as the metabolites produced by the gut microbiota, directly and indirectly, effect this axis. Microbial-derived metabolisms enter the bloodstream and penetrate the BBB and also effect on the EECs. EECs produce neurotransmitters that act on the axis through ENS, Signaling through the vagus nerve. Due to obesity and dysbiosis, increased intestinal permeability (Leaky Gut) and LPS cross the intestinal barrier and cause endotoxemia. SCFAs, short-chain fatty acids; LPS, lipopolysaccharide; BBB, blood-brain barrier; EEC, enteroendocrine cell; ENS, enteric nervous system; CCK, cholecystokinin; PYY, peptide YY; GLP-1, glucagon-like peptide; NTS, nucleus of tractus solitarius
Figure 3
Figure 3
The gut microbiota affects feeding behavior through the homeostatic pathway. This pathway includes the processing of signals from leptin and microbial-derived peptides, CCK, GLP-1, PYY, and ghrelin. Changes in the composition of the gut microbiota (dysbiosis) can affect the dopaminergic pathway. ARC, arcuate nucleus; POMC, pro-opiomelanocortin; CART, cocaine- and amphetamine-regulated transcript; NPY, neuropeptide Y; AgRP, agouti-related protein; SCFAs, short-chain fatty acids; PYY, peptide YY; CCK, cholecystokinin; GLP-1, glucagon-like peptide-1; EEC, enteroendocrine cell
Figure 3
Figure 3
Immunomodulation mechanisms of probiotics. Probiotics interact with epithelial cells, DCs, macrophages, B cells, Treg and Peyer's patches. DCs, dendritic cells; B cell, B lymphocytes; Treg, regulatory T cells; T cell, T lymphocytes
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