scholarly journals Roles of Gut Microbiota and Metabolites in Pathogenesis of Functional Constipation

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jun-Ke Wang ◽  
Shu-Kun Yao
Keyword(s):  
Gut Microbiota ◽  
Peptide Yy ◽  
Strong Association ◽  
Gut Hormones ◽  
Functional Constipation ◽  
Short Chain Fatty Acids ◽  
Enteric Neurons ◽  
Slow Transit Constipation ◽  
Research Strategies ◽  
Transit Constipation

Functional constipation (FC), a condition characterized by heterogeneous symptoms (infrequent bowel movements, hard stools, excessive straining, or a sense of incomplete evacuation), is prevalent over the world. It is a multifactorial disorder and can be categorized into four subgroups according to different pathological mechanisms: normal transit constipation (NTC), slow transit constipation (STC), defecatory disorders (DD), and mixed type. Recently, growing evidence from human and animals has pointed that there was a strong association between gut microbiota and FC based on the brain-gut-microbiome axis. Studies have reported that the main characteristics of gut microbiota in FC patients were the relative decrease of beneficial bacteria such as Lactobacillus and Bifidobacterium, the relative increase of potential pathogens, and the reduced species richness. Gut microbiota can modulate gut functions through the metabolites of bacterial fermentation, among which short-chain fatty acids (SCFAs), secondary bile salts (BAs), and methane occupied more important positions and could trigger the release of gut hormones from enteroendocrine cells (EECs), such as 5-hydroxytryptamine (5-HT), peptide YY (PYY), and glucagon-like peptide-1 (GLP-1). Subsequently, these gut hormones can influence gut sensation, secretion, and motility, primarily through activating specific receptors distributed on smooth muscle cells, enteric neurons, and epithelial cells. However, research findings were inconsistent and even conflicting, which may be partially due to various confounding factors. Future studies should take the associated confounders into consideration and adopt multiomics research strategies to obtain more complete conclusions and to provide reliable theoretical support for exploring new therapeutic targets.

Autoimmune encephalitis and gastrointestinal dysmotility: achalasia, gastroparesis, and slow transit constipation

2020 ◽  
Vol 58 (10) ◽  
pp. 975-981
Author(s):  
Thomas Frieling ◽  
Christian Kreysel ◽  
Michael Blank ◽  
Dorothee Müller ◽  
Ilka Melchior ◽  
...  
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Autoimmune Encephalitis ◽  
Enteric Neurons ◽  
Slow Transit Constipation ◽  
Gastrointestinal Dysmotility ◽  
Slow Transit ◽  
Small Intestinal ◽  
Interdigestive Motility ◽  
Cells Of Cajal ◽  
Transit Constipation

Abstract Background Neurological autoimmune disorders (NAD) are caused by autoimmune inflammation triggered by specific antibody subtypes. NAD may disturb the gut-brain axis at several levels including brain, spinal cord, peripheral, or enteric nervous system. Case report We present a case with antinuclear neuronal Hu (ANNA-1)- and antiglial nuclear (SOX-1) autoimmune antibody-positive limbic encephalitis and significant gastrointestinal dysmotility consisting of achalasia type II, gastroparesis, altered small intestinal interdigestive motility, and severe slow transit constipation. The autoantibodies of the patient’s serum labeled enteric neurons and interstitial cells of Cajal but no other cells in the gut wall. Achalasia was treated successfully by pneumatic cardia dilation and gastrointestinal dysmotility successfully with prucalopride. Conclusion NAD may disturb gastrointestinal motility by altering various levels of the gut-brain axis.

scholarly journals Gut Microbiota Alterations from Three-Strain Yogurt Formulation Treatments in Slow-Transit Constipation

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Xiao-Ran Li ◽  
Chen-Jian Liu ◽  
Xiao-Dan Tang ◽  
He-Ming Zhang ◽  
Yi-Yong Luo ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Gut Microbiota ◽  
Short Chain Fatty Acid ◽  
Intestinal Bacteria ◽  
Chain Fatty Acid ◽  
Slow Transit Constipation ◽  
Butanoic Acid ◽  
Treatment Groups ◽  
Slow Transit ◽  
Transit Constipation

The objective of this study was to evaluate the effects of a three-strain yogurt formulation in slow-transit constipation (STC) patients. Each individual in both treatment groups consumed 250 mL of the formulated yogurt daily for a week (7 days), and fecal samples were collected for gut microbiota and short-chain fatty acid (SCFA) analyses. A significant increase in the defection frequency (p<0.001) and bacterial diversity (p=0.027) at the 100% sequence homology level and a decrease in the concentrations of acetic acid (p=0.014), propionic acid (p=0.019), and butanoic acid (p=0.005) were observed after the STC patients consumed three-strain yogurt formulation. In addition, the consumption of the three-strain yogurt formulation significantly altered the composition of the intestinal bacteria in the STC patients. The relative abundances of 23 genera in the top dominating genera were altered significantly after the STC patients consumed the yogurt. In summary, the consumption of 250 mL day− the three-strain yogurt formulation described in this study can play a role in improving the symptoms of STC.

Plasma Cholecystokinin, Plasma Peptide YY and Gallbladder Motility in Patients with Slow Transit Constipation: Effect of Intestinal Stimulation

Digestion ◽  
2000 ◽  
Vol 62 (2-3) ◽  
pp. 185-193 ◽  
Author(s):  
Roland M.H.G. Mollen ◽  
Wim P.M. Hopman ◽  
Han H.C. Kuijpers ◽  
Jan B.M.J. Jansen
Keyword(s):  
Peptide Yy ◽  
Gallbladder Motility ◽  
Slow Transit Constipation ◽  
Plasma Cholecystokinin ◽  
Slow Transit ◽  
Transit Constipation

scholarly journals The effects of yam gruel on lowering fasted blood glucose in T2DM rats

2020 ◽  
Vol 15 (1) ◽  
pp. 763-773
Author(s):  
Xinjun Lin ◽  
Zongting Luo ◽  
Shuqin Pang ◽  
Carol Chunfeng Wang ◽  
Li Ge ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gut Microbiota ◽  
Peptide Yy ◽  
Short Chain Fatty Acids ◽  
Scientific Basis ◽  
Probiotic Bacteria ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled

AbstractThere is increasing evidence of the linkage between type 2 diabetes mellitus (T2DM) and gut microbiota. Based on our previous studies, we investigated the hypoglycemic mechanisms of yam gruel to provide a scientific basis for its popularization and application. Wistar rats were randomly divided into control and T2DM model groups. Rats in the model group were stimulated by a high-sugar/high-fat diet combined with an intraperitoneal injection of streptozotocin to induce T2DM. The T2DM rats were further subdivided randomly into three groups: (1) DM, (2) DM + yam gruel, and (3) DM + metformin. After 4 weeks of intervention, the changes in gut microbiota, short-chain fatty acids (SCFAs) (acetic acid, propionic acid, and butyric acid), the expression of G protein-coupled receptor 43 (GPR43), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and fasted blood glucose (FBG) levels were observed. Yam gruel intervention elevated the abundance of probiotic bacteria and increased the expression of SCFAs, GPR43 receptor, GLP-1, and PYY. It also reduced FBG levels. We conclude that yam gruel can lower FBG by promoting the growth of probiotic bacteria, increasing the content of SCFAs, and enhancing the expression of GPR43 receptor to increase the content of GLP-1 and PYY in serum.

scholarly journals Role of Gut Microbiota and Their Metabolites on Atherosclerosis, Hypertension and Human Blood Platelet Function: A Review

2020 ◽  
Author(s):  
Asim K Duttaroy
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Human Blood ◽  
Blood Platelets ◽  
Strong Association ◽  
Plasma Lipid ◽  
Blood Platelet ◽  
Short Chain Fatty Acids ◽  
Cardiac Events ◽  
Cvd Risk

Emerging data have demonstrated a strong association between the gut microbiota and the development of cardiovascular disease (CVD) risk factors such as atherosclerosis, inflammation, obesity, insulin resistance, platelet hyperactivity, and plasma lipid abnormalities. Several studies in humans and animal models have demonstrated an association between gut microbial metabolites, such as trimethylamine-N-oxide (TMAO), short-chain fatty acids, and bile acid metabolites, amino acid breakdown products, with CVD. Human blood platelets are a critical contributor to the hemostatic process. Besides, these blood cells play a crucial role in developing atherosclerosis and, finally, contribute to cardiac events. Since the TMAO, and other metabolites of the gut microbiota, are associated with platelet hyperactivity, lipid disorders, and oxidative stress, the diet-gut microbiota interactions have become an important research area in the cardiovascular field. Platelets became hyperactive in people with diabetes mellitus, sedentary lifestyle, obesity, and insulin resistance and exhibited increased sensitivity at a baseline level and in response to agonists, ultimately contributing to increased aggregation plaque development. In addition to these factors, TMAO also contributes to platelet hyperactivity. Several approaches are now suggested to reduce plasma TMAO levels, such as microbiota modulation using probiotics, prebiotics, and oral broad-spectrum antibiotics. This review describes the association between microbiota-derived metabolites and CVD development.

scholarly journals Effect of fecal microbiota transplantation in patients with slow transit constipation and the relative mechanisms based on the protein digestion and absorption pathway

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Lulu Xie ◽  
Chen Xu ◽  
Yadong Fan ◽  
Yuwei Li ◽  
Ying Wang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Slow Transit Constipation ◽  
Hamilton Depression Scale ◽  
Protein Digestion ◽  
Slow Transit ◽  
Transit Constipation ◽  
16 S Rrna ◽  
Absorption Pathways

Abstract Background Fecal microbiota transplantation (FMT) is considered an effective treatment for slow transit constipation (STC); nevertheless, the mechanism remains unclear. Methods In this study, eight patients with STC were selected according to the inclusion and exclusion criteria; they then received three treatments of FMT. The feces and serum of STC patients were collected after each treatment and analyzed by integrating 16 s rRNA microbiome and metabolomic analyses. Results The results showed that the percentage of clinical improvement reached 62.5% and the rates of patients’ clinical remission achieved 75% after the third treatment. At the same time, FMT improved the Wexner constipation scale (WCS), the Gastrointestinal Quality-of-Life Index (GIQLI) and Hamilton Depression Scale (HAMD). Fecal microbiome alpha diversity and beta diversity altered significantly after FMT. Analysis of the 16 s rRNA microbiome showed that the numbers of Bacteroidetes (Prevotell/Bacteroides) and Firmicute (Roseburia/Blautia) decreased, whereas Actinobacteria (Bifidobacterium), Proteobacteria (Escherichia), and Firmicute (Lactobacillus) increased after FMT. The metabolomics analyses showed that the stool of FMT-treated patients were characterized by relatively high levels of N-Acetyl-L-glutamate, gamma-L-glutamyl-L-glutamic acid, Glycerophosphocholine, et al., after FMT. Compared with baseline, the serum of treated patients was characterized by relatively high levels of L-Arginine, L-Threonine, Ser-Arg, Indoleacrylic acid, Phe-Tyr, 5-L-Glutamyl-L-alanine, and lower levels of Erucamide after the treatment. The correlation analysis between the metabolites and gut microbiota showed a significant correlation. For example, L-Arginine was positively correlated with lactobacillus, et al. L-Threonine was positively correlated with Anaerovibrio, Sediminibacterium but negatively correlated with Phascolarctobacterium. Erucamide had significant negative correlations with Sediminibacterium and Sharpea, while being positively correlated with Phascolarctobacterium. Enriched KEGG pathways analysis demonstrated that the protein digestion and absorption pathways gradually upregulated with the increase of FMT frequency. The L-Arginine and L-Threonine were also involved in the pathway. A large amount of Na + was absorbed in the pathway, so that it might increase mucus secretion and electrical excitability of GI smooth muscle. Conclusions Therefore, we speculated that FMT changed the patients’ gut microbiota and metabolites involved in the protein digestion and absorption pathways, thereby improving the symptoms of STC. Study on the effectiveness and safety of FMT in the treatment of STC. The study was reviewed and approved by Ethics Committee of Tianjin People's Hospital (ChiCTR2000033227) in 2020.

Peptide YY release after colectomy in slow transit constipation

2004 ◽  
Vol 39 (8) ◽  
pp. 727-730 ◽  
Author(s):  
W. P. M. Hopman ◽  
R. M. H. G. Mollen ◽  
J. H. C. Kuijpers ◽  
J. B. M. J. Jansen
Keyword(s):  
Peptide Yy ◽  
Slow Transit Constipation ◽  
Slow Transit ◽  
Transit Constipation

scholarly journals GPR41/FFAR3 and GPR43/FFAR2 as Cosensors for Short-Chain Fatty Acids in Enteroendocrine Cells vs FFAR3 in Enteric Neurons and FFAR2 in Enteric Leukocytes

Endocrinology ◽  
2013 ◽  
Vol 154 (10) ◽  
pp. 3552-3564 ◽  
Author(s):  
Mark K. Nøhr ◽  
Maria H. Pedersen ◽  
Andreas Gille ◽  
Kristoffer L. Egerod ◽  
Maja S. Engelstoft ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Small Intestine ◽  
Fatty Acid ◽  
Peptide Yy ◽  
Large Population ◽  
Short Chain Fatty Acids ◽  
Enteroendocrine Cells ◽  
Enteric Neurons ◽  
Short Chain ◽  
Free Fatty Acid Receptor

The expression of short-chain fatty acid receptors GPR41/FFAR3 and GPR43/ free fatty acid receptor 2 (FFAR2) was studied in the gastrointestinal tract of transgenic monomeric red fluorescent protein (mRFP) reporter mice. In the stomach free fatty acid receptor 3 (FFAR3)-mRFP was expressed in a subpopulation of ghrelin and gastrin cells. In contrast, strong expression of FFAR3-mRFP was observed in all cholecystokinin, glucose-dependent insulinotropic peptide (GIP), and secretin cells of the proximal small intestine and in all glucagon-like peptide-1 (GLP-1), peptide YY, and neurotensin cells of the distal small intestine. Throughout the colon and rectum, FFAR3-mRFP was strongly expressed in the large population of peptide YY and GLP-1 cells and in the neurotensin cells of the proximal colon. A gradient of expression of FFAR3-mRFP was observed in the somatostatin cells from less than 5% in the stomach to more than 95% in the rectum. Substance P-containing enterochromaffin cells displayed a similar gradient of FFAR3-mRFP expression throughout the small intestine. Surprisingly, FFAR3-mRFP was also expressed in the neuronal cells of the submucosal and myenteric ganglia. Quantitative PCR analysis of fluorescence-activated cell sorting (FACS) purified FFAR3-mRFP positive cells confirmed the coexpression with the various peptide hormones as well as key neuronal marker proteins. The FFAR2-mRFP reporter was strongly expressed in a large population of leukocytes in the lamina propria of in particular the small intestine but surprisingly only weakly in a subpopulation of enteroendocrine cells. Nevertheless, synthetic ligands specific for either FFAR3 or FFAR2 each released GLP-1 from colonic crypt cultures and the FFAR2 agonist mobilized intracellular Ca2+ in FFAR2 positive enteroendocrine cells. It is concluded that FFAR3-mRFP serves as a useful marker for the majority of enteroendocrine cells of the small and large intestine and that FFAR3 and FFAR2 both act as sensors for short-chain fatty acids in enteroendocrine cells, whereas FFAR3 apparently has this role alone in enteric neurons and FFAR2 in enteric leukocytes.

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