scholarly journals Obesity as a risk factor for diseases of the digestive system

2021 ◽  
Vol 93 (8) ◽  
pp. 954-962
Author(s):  
Dmitry N. Andreev ◽  
Yury A. Kucheryavyy
Keyword(s):  
Fatty Acids ◽  
Adult Population ◽  
Interleukin 1 ◽  
Short Chain Fatty Acids ◽  
Systemic Circulation ◽  
Active Forms Of Oxygen ◽  
Alcoholic Fatty Liver ◽  
Quantitative Changes ◽  
Irritable Bowel ◽  
Factor C

Currently, the global prevalence of obesity among the worlds adult population is about 650 million people, which makes it possible to consider this chronic metabolic disease as a non-infectious pandemic of the 21st century. It has been proven that obesity is associated with several gastroenterological diseases, while the mechanisms of these associations are extremely heterogeneous and multifactorial. Hypertrophy and hyperplasia of adipocytes in obesity lead to a change in the profile of adipokine production (a decrease in adiponectin, an increase in leptin), an increase in the production of pro-inflammatory cytokines (interleukin-1, 6, 8, tumor necrosis factor ), C-reactive protein, free fatty acids, as well as active forms of oxygen (superoxide radicals, H2O2). All the above induces the development of chronic slowly progressive inflammation, oxidative stress, and insulin resistance. In addition, peptides secreted by adipocytes (adiponectin, leptin, nesfatin-1 and apelin) can modulate gastrointestinal motility, acting both centrally and peripherally. The qualitative and quantitative changes in the intestinal microbiota observed in obese patients (increased Firmicutes and decreased Bacteroidetes) lead to a decrease in the production of short-chain fatty acids and an increase in the intestinal permeability due to disruption of intercellular tight junctions, which leads to increased translocation of bacteria and endotoxins into the systemic circulation. Numerous studies have demonstrated the association of obesity with diseases of the esophagus (gastroesophageal reflux disease, Barretts esophagus, esophageal adenocarcinoma, esophageal motility disorders), stomach (functional dyspepsia, stomach cancer), gallbladder (cholelithiasis, gallbladder cancer), pancreas (acute pancreatitis, pancreatic cancer), liver (non-alcoholic fatty liver disease, hepatocellular carcinoma), intestine (diverticular disease, irritable bowel syndrome, colorectal cancer).

scholarly journals Modulation of serotonin in the gut-liver neural axis ameliorates the fatty and fibrotic changes in non-alcoholic fatty liver

2021 ◽  
Vol 14 (3) ◽  
pp. dmm048922
Author(s):  
Masayoshi Ko ◽  
Kenya Kamimura ◽  
Takashi Owaki ◽  
Takuro Nagoya ◽  
Norihiro Sakai ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Tight Junction ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Neural Signal ◽  
Alcoholic Fatty Liver ◽  
Serotonin Antagonist ◽  
Neural Axis

ABSTRACTThe etiology of non-alcoholic fatty liver disease (NAFLD) consists of various factors, including neural signal pathways. However, the molecular mechanisms of the autonomic neural signals influencing NAFLD progression have not been elucidated. Therefore, we examined the involvement of the gut-liver neural axis in NAFLD development and tested the therapeutic effect of modulation of this axis in this study. To test the contribution of the gut-liver neural axis, we examined NAFLD progression with respect to body weight, hepatic steatosis, fibrosis, intestinal tight junction, microbiota and short-chain fatty acids in NAFLD models of choline-deficient defined L-amino-acid and high-fat diet-fed mice with or without blockades of autonomic nerves from the liver. Blockade of the neural signal from the liver to the gut in these NAFLD mice models ameliorated the progression of liver weight, hepatic steatosis and fibrosis by modulating serotonin expression in the small intestine. It was related to the severity of the liver pathology, the tight junction protein expression, microbiota diversity and short-chain fatty acids. These effects were reproduced by administrating serotonin antagonist, which ameliorated the NAFLD progression in the NAFLD mice models. Our study demonstrated that the gut-liver neural axis is involved in the etiologies of NAFLD progression and that serotonin expression through this signaling network is the key factor of this axis. Therefore, modulation of the gut-liver neural axis and serotonin antagonist ameliorates fatty and fibrotic changes in non-alcoholic fatty liver, and can be a potential therapeutic target of NAFLD.This article has an associated First Person interview with the first author of the paper.

scholarly journals Gut Microbiota-Derived Metabolites in Irritable Bowel Syndrome

2021 ◽  
Vol 11 ◽  
Author(s):  
Lin Xiao ◽  
Qin Liu ◽  
Mei Luo ◽  
Lishou Xiong
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Irritable Bowel Syndrome ◽  
Gut Microbiota ◽  
Short Chain Fatty Acids ◽  
Functional Bowel Disorder ◽  
Irritable Bowel ◽  
The Brain ◽  
Bowel Disorder

Irritable bowel syndrome (IBS) is the most common functional bowel disorder worldwide and is associated with visceral hypersensitivity, gut motility, immunomodulation, gut microbiota alterations, and dysfunction of the brain-gut axis; however, its pathophysiology remains poorly understood. Gut microbiota and its metabolites are proposed as possible etiological factors of IBS. The aim of our study was to investigate specific types of microbiota-derived metabolites, especially bile acids, short-chain fatty acids, vitamins, amino acids, serotonin and hypoxanthine, which are all implicated in the pathogenesis of IBS. Metabolites-focused research has identified multiple microbial targets relevant to IBS patients, important roles of microbiota-derived metabolites in the development of IBS symptoms have been established. Thus, we provide an overview of gut microbiota and their metabolites on the different subtypes of IBS (constipation-predominant IBS-C, diarrhea-predominant IBS-D) and present controversial views regarding the role of microbiota in IBS.

scholarly journals Fecal Bile Acids and Fecal Short Chain Fatty Acids in Patients with Irritable Bowel Syndrome and Control Volunteers

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Chirag Patel ◽  
Carolyn Lockett ◽  
Huiping Xu ◽  
Andrea Shin
Keyword(s):  
Fatty Acids ◽  
Irritable Bowel Syndrome ◽  
Organic Acids ◽  
Bile Acids ◽  
Short Chain Fatty Acids ◽  
Small Sample ◽  
Short Chain ◽  
Fecal Bile Acids ◽  
Irritable Bowel ◽  
Chain Fatty Acids

Background and Aims: Fecal bile acids (BAs), short chain fatty acids (SCFAs), and gut microbiome may be implicated in irritable bowel syndrome (IBS) pathophysiology. Our aim was to compare fecal organic acids between IBS with constipation (IBS-C), IBS with diarrhea (IBS-D), and controls.   Methods: Stool samples were collected from 17 controls, 5 IBS-C, and 5 IBS-D volunteers during a 4-day high fat diet. Aliquots were stored for future analysis of the fecal microbiota. Fecal SCFA and BA analyses were conducted at the Metabolite Profiling Facility at Purdue University and Laboratory Medicine and Pathology at Mayo Clinic. We compared SCFA and BA levels among groups using the Wilcoxon rank sum test. Gamma and linear regression were used to compare SCFAs and BAs adjusting for age and body mass index (BMI).  Results: Fecal acetate levels (mean+SD, µg/mg) were higher in IBS-C (11.3±7) than in controls (6.1±3.3) or IBS-D (7.7±2), although not statistically significant (p=0.19). Total fecal BAs (median [IQR], %) were higher in IBS-D (675 [484-778]) than in controls (342 [130-640]) or IBS-C (321.5 (34.5-718); however, differences were not significant. No significant differences were observed in BAs or SCFAs between groups in multivariate analyses.  Conclusion: We are unable to show significant differences in organic acid levels in IBS and controls. Lack of association may be due to small sample size. Future investigation of larger patient numbers with incorporation of transit and microbiome analyses may shed further light on the role of organic acids in IBS to identify new biomarkers and treatment targets.

Mo1323 SEX-BASED DIFFERENCES IN FECAL SHORT-CHAIN FATTY ACIDS IN IRRITABLE BOWEL SYNDROME PATINETS AND A SCORECARD TO ASSIST DIAGNOSIS

2020 ◽  
Vol 158 (6) ◽  
pp. S-849-S-850
Author(s):  
Qinghua Sun ◽  
Zuojing Liu ◽  
Lu Zhang ◽  
Lijin Song ◽  
Hui Wei ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Irritable Bowel Syndrome ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Irritable Bowel ◽  
Chain Fatty Acids

scholarly journals Chemical and molecular factors in irritable bowel syndrome: current knowledge, challenges, and unanswered questions

2016 ◽  
Vol 311 (5) ◽  
pp. G777-G784 ◽  
Author(s):  
Michael Camilleri ◽  
Ibironke Oduyebo ◽  
Houssam Halawi
Keyword(s):  
Fatty Acids ◽  
Irritable Bowel Syndrome ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Short Chain Fatty Acids ◽  
Mucosal Barrier ◽  
Future Research ◽  
Enteroendocrine Cell ◽  
The Central Nervous System ◽  
Irritable Bowel

Several chemical and molecular factors in the intestine are reported to be altered and to have a potentially significant role in irritable bowel syndrome (IBS), particularly in IBS with diarrhea. These include bile acids; short-chain fatty acids; mucosal barrier proteins; mast cell products such as histamine, proteases, and tryptase; enteroendocrine cell products; and mucosal mRNAs, proteins, and microRNAs. This article reviews the current knowledge and unanswered questions in the pathobiology of the chemical and molecular factors in IBS. Evidence continues to point to significant roles in pathogenesis of these chemical and molecular mechanisms, which may therefore constitute potential targets for future research and therapy. However, it is still necessary to address the interaction between these factors in the gut and to appraise how they may influence hypervigilance in the central nervous system in patients with IBS.

scholarly journals Alterations in short-chain fatty acids and serotonin in irritable bowel syndrome: a systematic review and meta-analysis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mei Luo ◽  
Xiaojun Zhuang ◽  
Zhenyi Tian ◽  
Lishou Xiong
Keyword(s):  
Fatty Acids ◽  
Irritable Bowel Syndrome ◽  
Meta Analysis ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Cochrane Library ◽  
Case Control Studies ◽  
Mean Differences ◽  
Irritable Bowel ◽  
Chain Fatty Acids

Abstract Background Short-chain fatty acids (SCFAs) and serotonin (5-hydroxytryptamine, 5-HT) may be associated with the pathogenesis of irritable bowel syndrome (IBS). There are some reports of alterations in SCFAs and 5-HT in IBS, but their results are inconsistent. We aimed to perform a meta-analysis to assess alterations in SCFAs and 5-HT in IBS patients and their potential role in the abnormal brain-gut-microbiota (BGM) axis. Methods Case–control studies detecting SCFAs and 5-HT in IBS patients were identified from PubMed, Web of Science, Cochrane Library, and Scopus databases to identify relevant articles up to September 2018. The standardized mean differences (SMDs) with 95% confidence intervals (CIs) of SCFAs and 5-HT were calculated by REVIEW MANAGER 5.3 to evaluate the alterations of 5-HT and SCFAs in IBS. Results Five studies on SCFAs and 5 on 5-HT in IBS patients were included. As compared to healthy controls (HCs), the SMDs of 5-HT in IBS patients was 2.35 (95% CI 0.46–4.24) and the SMDs of total SCFAs, acetic acid, propionic acid, and butyric acid in IBS patients were − 0.01 (95% CI − 0.57–0.55), − 0.04 (95% CI − 0.55–0.47), 0.07 (95% CI − 0.45–0.60), and − 0.00 (95% CI − 0.49–0.49), respectively. Conclusions There was an increase in 5-HT in blood of IBS patients, indicating the increased 5-HT in blood may be involved in IBS pathogenesis. However, there were no significant differences in SCFAs in feces between IBS patients and HCs. But the study did not differentiate between subgroups of IBS. These findings might provide insight for future studies of the BGM axis in the pathogenesis of IBS. Mei Luo and Xiaojun Zhuang contributed equally to the writing of this article

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