• Journal of Animal Science and Technology
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• v.64 no.4
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• pp.671-695
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• 2022

The gastrointestinal tract is a complex ecosystem that contains a large number of microorganisms with different metabolic capacities. Modulation of the gut microbiome can improve the growth and promote health in pigs. Crosstalk between the host, diet, and the gut microbiome can influence the health of the host, potentially through the production of several metabolites with various functions. Short-chain and branched-chain fatty acids, secondary bile acids, polyamines, indoles, and phenolic compounds are metabolites produced by the gut microbiome. The gut microbiome can also produce neurotransmitters (such as γ-aminobutyric acid, catecholamines, and serotonin), their precursors, and vitamins. Several studies in pigs have demonstrated the importance of the gut microbiome and its metabolites in improving growth performance and feed efficiency, alleviating stress, and providing protection from pathogens. The use of probiotics is one of the strategies employed to target the gut microbiome of pigs. Promising results have been published on the use of probiotics in optimizing pig production. This review focuses on the role of gut microbiome-derived metabolites in the performance of pigs and the effects of probiotics on altering the levels of these metabolites.

• Biomolecules & Therapeutics
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• v.32 no.4
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• pp.403-423
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• 2024

The human gastrointestinal (GI) tract houses a diverse microbial community, known as the gut microbiome comprising bacteria, viruses, fungi, and protozoa. The gut microbiome plays a crucial role in maintaining the body's equilibrium and has recently been discovered to influence the functioning of the central nervous system (CNS). The communication between the nervous system and the GI tract occurs through a two-way network called the gut-brain axis. The nervous system and the GI tract can modulate each other through activated neuronal cells, the immune system, and metabolites produced by the gut microbiome. Extensive research both in preclinical and clinical realms, has highlighted the complex relationship between the gut and diseases associated with the CNS, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This review aims to delineate receptor and target enzymes linked with gut microbiota metabolites and explore their specific roles within the brain, particularly their impact on CNS-related diseases.

• Microbiology and Biotechnology Letters
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• v.51 no.4
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• pp.531-534
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• 2023

We report the draft genome sequence of the yeast strain Hormonema macrosporum POB-4, capable of producing the biosurfactant glycocholic acid, one of the bile acids. A majority of genes with known function were associated with metabolism and transport of amino acid and carbohydrate as well as secondary metabolites biosynthesis, transport, and catabolism. We observed genes of eleven C-N hydrolases and two CoA transferases which have been reported to be involved in the biosynthesis of glycocholic acid. Further experimental studies can help to elucidate the specific genes responsible for biosurfactant production in strain POB-4.

• Journal of Ginseng Research
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• v.46 no.6
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• pp.780-789
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• 2022

Background: Incretin impairment, characterized by insufficient secretion of L-cell-derived glucagon-like peptide-1 (GLP-1), is a defining step of type 2 diabetes mellitus (T2DM). Ginsenoside compound K (CK) can stimulate GLP-1 secretion; however, the potential mechanism underlying this effect has not been established. Methods: CK (40 mg/kg) was administered orally to male db/db mice for 4 weeks. The body weight, oral glucose tolerance, GLP-1 secretion, gut microbiota sequencing, bile acid (BA) profiles, and BA synthesis markers of each subject were then analyzed. Moreover, TGR5 expression was evaluated by immunoblotting and immunofluorescence, and L-cell lineage markers involved in L-cell abundance were analyzed. Results: CK ameliorated obesity and impaired glucose tolerance in db/db mice by altering the gut microbiota, especially Ruminococcaceae family, and this changed microbe was positively correlated with secondary BA synthesis. Additionally, CK treatment resulted in the up-regulation of CYP7B1 and CYP27A1 and the down-regulation of CYP8B1, thereby shifting BA biosynthesis from the classical pathway to the alternative pathway. CK altered the BA pool by mainly increasing LCA and DCA. Furthermore, CK induced L-cell number expansion leading to enhanced GLP-1 release through TGR5 activation. These increases were supported by the upregulation of genes governing GLP-1 secretion and L-cell differentiation. Conclusions: The results indicate that CK improves glucose homeostasis by increasing L-cell numbers, which enhances GLP-1 release through a mechanism partially mediated by the gut microbiota-BA-TGR5 pathway. Therefore, that therapeutic attempts with CK might be useful for patients with T2DM.