scholarly journals The role of gut microbiota in the development of obesity and its metabolic profile (Part II)

2019 ◽  
Vol 14 (2) ◽  
Author(s):  
Natalia Volkova ◽  
Liliya Ganenko ◽  
Sergey Golovin
2022 ◽  
Vol 8 ◽  
Author(s):  
Zhifeng Wu ◽  
Wei Cheng ◽  
Zhenyu Wang ◽  
Shuaifei Feng ◽  
Huicong Zou ◽  
...  

There is an interaction and bidirectional selection between dietary intake and gut microbiota due to the different efficiency of nutrients in the gut. The nutritional composition of germ-free (GF) diets differs significantly from specific pathogen-free (SPF) diets. There is, however, no data revealing how SPF animals from the same microbial background respond to them and if they affect the host. We examined the growth of SPF mice on the GF diet and found that it reduced body weight, intestinal length and intestinal morphology. Interestingly, the GF diet increased the level of pro-inflammatory bacteria in the gut of SPF mice, including Proteobacteria, Burkholderiaceae, Alloprevotella and Parasutterella. Furthermore, GF diets caused significant increases in malondialdehyde (MDA), IL-1β, IL-6, and D-lactate levels in the serum of SPF mice and significantly altered their serum metabolic profile, especially amino acid metabolism. In conclusion, GF diets are not suitable for the growth and development of SPF mice. These findings, based on the role of gut microbiota in diet selection, provide new insights into the scientific and rational use of experimental animal diets.


2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Natalia Volkova ◽  
Liliya Ganenko ◽  
Sergey Golovin ◽  
Elena Beresniak

Author(s):  
Dong-Yu Kan ◽  
Su-Juan Li ◽  
Chen-Chen Liu ◽  
Ren-Rong Wu

Schizophrenia is a chronic and severe mental disorder with antipsychotics as primary medications, but the antipsychotic-induced metabolic side effects may contribute to the elevated risk of overall morbidity and mortality in patients with psych-iatric diseases. With the development in sequencing technology and bioinformatics, dysbiosis has been shown to contribute to body weight gain and metabolic dysfunction. However, the role of gut microbiota in the antipsychotic-induced metabolic alteration remains unknown. In this paper, we reviewed the recent studies of the gut microbiota with psychiatric disorders and antipsychotic-induced metabolic dysfunction. Patients with neuropsychiatric disorders may have a different composi-tion of gut microbiota compared with healthy controls. In addition, it seems that the use of antipsychotics is concurrently associated with both altered composition of gut microbiota and metabolic disturbance. Further study is needed to address the role of gut microbiota in the development of neuropsychiatric disorders and antipsychotic-induced metabolic disturbance, to develop novel therapeutics for both neuropsychiatric disorders and metabolic dysfunction.


2020 ◽  
Vol 19 (7) ◽  
pp. 509-526
Author(s):  
Qin Huang ◽  
Fang Yu ◽  
Di Liao ◽  
Jian Xia

: Recent studies implicate microbiota-brain communication as an essential factor for physiology and pathophysiology in brain function and neurodevelopment. One of the pivotal mechanisms about gut to brain communication is through the regulation and interaction of gut microbiota on the host immune system. In this review, we will discuss the role of microbiota-immune systeminteractions in human neurological disorders. The characteristic features in the development of neurological diseases include gut dysbiosis, the disturbed intestinal/Blood-Brain Barrier (BBB) permeability, the activated inflammatory response, and the changed microbial metabolites. Neurological disorders contribute to gut dysbiosis and some relevant metabolites in a top-down way. In turn, the activated immune system induced by the change of gut microbiota may deteriorate the development of neurological diseases through the disturbed gut/BBB barrier in a down-top way. Understanding the characterization and identification of microbiome-immune- brain signaling pathways will help us to yield novel therapeutic strategies by targeting the gut microbiome in neurological disease.


2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S42-S42
Author(s):  
Kohei Sugihara ◽  
Nobuhiko Kamada

Abstract Background Recent accumulating evidence suggests that amino acids have crucial roles in the maintenance of intestinal homeostasis. In inflammatory bowel disease (IBD), amino acid metabolism is changed in both host and the gut microbiota. Among amino acids, L-serine plays a central role in several metabolic processes that are essential for the growth and survival of both mammalian and bacterial cells. However, the role of L-serine in intestinal homeostasis and IBD remains incompletely understood. In this study, we investigated the effect of dietary L-serine on intestinal inflammation in a murine model of colitis. Methods Specific pathogen-free (SPF) mice were fed either a control diet (amino acid-based diet) or an L-serine-deficient diet (SDD). Colitis was induced by the treatment of dextran sodium sulfate (DSS). The gut microbiome was analyzed by 16S rRNA sequencing. We also evaluate the effect of dietary L-serine in germ-free mice and gnotobiotic mice that were colonized by a consortium of non-mucolytic bacterial strains or the consortium plus mucolytic bacterial strains. Results We found that the SDD exacerbated experimental colitis in SPF mice. However, the severity of colitis in SDD-fed mice was comparable to control diet-fed mice in germ-free condition, suggesting that the gut microbiota is required for exacerbation of colitis caused by the restriction of dietary L-serine. The gut microbiome analysis revealed that dietary L-serine restriction fosters the blooms of a mucus-degrading bacterium Akkermansia muciniphila and adherent-invasive Escherichia coli in the inflamed gut. Consistent with the expansion of mucolytic bacteria, SDD-fed mice showed a loss of the intestinal mucus layer. Dysfunction of the mucus barrier resulted in increased intestinal permeability, thereby leading to bacterial translocation to the intestinal mucosa, which subsequently increased the severity of colitis. The increased intestinal permeability and subsequent bacterial translocation were observed in SDD-fed gnotobiotic mice that colonized by mucolytic bacteria. In contrast, dietary L-serine restriction did not alter intestinal barrier integrity in gnotobiotic mice that colonized only by non-mucolytic bacteria. Conclusion Our results suggest that dietary L-serine regulates the integrity of the intestinal mucus barrier during inflammation by limiting the expansion of mucus degrading bacteria.


2019 ◽  
Vol 156 (6) ◽  
pp. S-1124
Author(s):  
Clara Caenepeel ◽  
Sara Vieira-Silva ◽  
Jorge F. Vázquez-Castellanos ◽  
Bram Verstockt ◽  
Marc Ferrante ◽  
...  

Bone ◽  
2020 ◽  
Vol 135 ◽  
pp. 115317 ◽  
Author(s):  
Jyotirmaya Behera ◽  
Jessica Ison ◽  
Suresh C. Tyagi ◽  
Neetu Tyagi

Fermentation ◽  
2021 ◽  
Vol 7 (1) ◽  
pp. 14
Author(s):  
Nelson Mota de Carvalho ◽  
Diana Luazi Oliveira ◽  
Mayra Anton Dib Saleh ◽  
Manuela Pintado ◽  
Ana Raquel Madureira

The use of fecal inoculums for in vitro fermentation models requires a viable gut microbiota, capable of fermenting the unabsorbed nutrients. Fresh samples from human donors are used; however, the availability of fresh fecal inoculum and its inherent variability is often a problem. This study aimed to optimize a method of preserving pooled human fecal samples for in vitro fermentation studies. Different conditions and times of storage at −20 °C were tested. In vitro fermentation experiments were carried out for both fresh and frozen inoculums, and the metabolic profile compared. In comparison with the fresh, the inoculum frozen in a PBS and 30% glycerol solution, had a significantly lower (p < 0.05) bacterial count (<1 log CFU/mL). However, no significant differences (p < 0.05) were found between the metabolic profiles after 48 h. Hence, a PBS and 30% glycerol solution can be used to maintain the gut microbiota viability during storage at −20 °C for at least 3 months, without interfering with the normal course of colonic fermentation.


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