Screening dietary fibres for fermentation characteristics and metabolic profiles using a rapidin vitroapproach: implications for irritable bowel syndrome
Abstract:The therapeutic value of specific fibres is partly dependent on their fermentation characteristics. Some fibres are rapidly degraded with generation of gases that induce symptoms in patients with irritable bowel syndrome (IBS), while more slowly- or non-fermentable fibres may be more suitable. More work is needed to profile a comprehensive range of fibre to determine suitability for IBS. Using a rapid in vitro fermentation model, gas production and metabolite profiles of a range of established and novel fibres… Show more
“…Reduced in IBD (293,297) Increased in IBS (248,302) Increased in UC (252) and in CD (293) Reduced in CD (252,298) Increased in Parkinson's disease (259) Increased in Alzheimer's disease (300) Decreased in autism spectrum disorder (301) Decreased in bipolar disorder (258) Increases 5-HT levels (232) Correlated with levels of serotonin (303) Veillonellaceae Increased in IBS (304,305) Increased in IBD (305,306) Increased in UC and CD (252) Decreased in autism spectrum disorder (256) Correlated with increased levels of serotonin (307) Lactobacillaceae Increased in IBS (248) Increased in IBD (297) Decreased in IBD (Lactobacillus) (250) Increased in CD and reduced in UC (252) Increased in Parkinson's disease (253,255,308) Decreased in Alzheimer's disease (251) Increased in Alzheimer's disease (300) Increased in autism spectrum disorder (257) Decreases TPH1, 5-THR 3 and 5-HTR 4 expression; and increases SERT expression…”
Disruption of the microbiota–gut–brain axis results in a wide range of pathologies that are affected, from the brain to the intestine. Gut hormones released by enteroendocrine cells to the gastrointestinal (GI) tract are important signaling molecules within this axis. In the search for the language that allows microbiota to communicate with the gut and the brain, serotonin seems to be the most important mediator. In recent years, serotonin has emerged as a key neurotransmitter in the gut–brain axis because it largely contributes to both GI and brain physiology. In addition, intestinal microbiota are crucial in serotonin signaling, which gives more relevance to the role of the serotonin as an important mediator in microbiota–host interactions. Despite the numerous investigations focused on the gut–brain axis and the pathologies associated, little is known regarding how serotonin can mediate in the microbiota–gut–brain axis. In this review, we will mainly discuss serotonergic system modulation by microbiota as a pathway of communication between intestinal microbes and the body on the microbiota–gut–brain axis, and we explore novel therapeutic approaches for GI diseases and mental disorders.
“…Reduced in IBD (293,297) Increased in IBS (248,302) Increased in UC (252) and in CD (293) Reduced in CD (252,298) Increased in Parkinson's disease (259) Increased in Alzheimer's disease (300) Decreased in autism spectrum disorder (301) Decreased in bipolar disorder (258) Increases 5-HT levels (232) Correlated with levels of serotonin (303) Veillonellaceae Increased in IBS (304,305) Increased in IBD (305,306) Increased in UC and CD (252) Decreased in autism spectrum disorder (256) Correlated with increased levels of serotonin (307) Lactobacillaceae Increased in IBS (248) Increased in IBD (297) Decreased in IBD (Lactobacillus) (250) Increased in CD and reduced in UC (252) Increased in Parkinson's disease (253,255,308) Decreased in Alzheimer's disease (251) Increased in Alzheimer's disease (300) Increased in autism spectrum disorder (257) Decreases TPH1, 5-THR 3 and 5-HTR 4 expression; and increases SERT expression…”
Disruption of the microbiota–gut–brain axis results in a wide range of pathologies that are affected, from the brain to the intestine. Gut hormones released by enteroendocrine cells to the gastrointestinal (GI) tract are important signaling molecules within this axis. In the search for the language that allows microbiota to communicate with the gut and the brain, serotonin seems to be the most important mediator. In recent years, serotonin has emerged as a key neurotransmitter in the gut–brain axis because it largely contributes to both GI and brain physiology. In addition, intestinal microbiota are crucial in serotonin signaling, which gives more relevance to the role of the serotonin as an important mediator in microbiota–host interactions. Despite the numerous investigations focused on the gut–brain axis and the pathologies associated, little is known regarding how serotonin can mediate in the microbiota–gut–brain axis. In this review, we will mainly discuss serotonergic system modulation by microbiota as a pathway of communication between intestinal microbes and the body on the microbiota–gut–brain axis, and we explore novel therapeutic approaches for GI diseases and mental disorders.
“…Briefly, plasma SCFAs were measured in 200 mL, and faecal SCFAs were measured from 1 g of faecal sample, all in The Gut Microbiome and Ambulatory Arterial Stiffness Index triplicates, as previously published, in an Agilent GC6890 gas chromatograph coupled to a flame-ionisation detector [25,26]. A coefficient of variation of ,10% within triplicate samples was used as a quality control measure.…”
Gut microbiota-derived metabolites, such as short-chain fatty acids (SCFAs) have vasodilator properties in animal and human ex vivo arteries. However, the role of the gut microbiota and SCFAs in arterial stiffness in humans is still unclear. Here we aimed to determine associations between the gut microbiome, SCFA and their G-protein coupled sensing receptors (GPCRs) in relation to human arterial stiffness.
MethodsAmbulatory arterial stiffness index (AASI) was determined from ambulatory blood pressure (BP) monitoring in 69 participants from regional and metropolitan regions in Australia (55.1% women; mean, 59.86 SD, 7.26 years of age). The gut microbiome was determined by 16S rRNA sequencing, SCFA levels by gas chromatography, and GPCR expression in circulating immune cells by real-time PCR.
ResultsThere was no association between metrics of bacterial a and b diversity and AASI or AASI quartiles in men and women. We identified two main bacteria taxa that were associated with AASI quartiles: Lactobacillus spp. was only present in the lowest quartile, while Clostridium spp. was present in all quartiles but the lowest. AASI was positively associated with higher levels of plasma, but not faecal, butyrate. Finally, we identified that the expression of GPR43 (FFAR2) and GPR41 (FFAR3) in circulating immune cells were negatively associated with AASI.
ConclusionsOur results suggest that arterial stiffness is associated with lower levels of the metabolite-sensing receptors GPR41/GPR43 in humans, blunting its response to BP-lowering metabolites such as butyrate. The role of Lactobacillus spp. and Clostridium spp., as well as butyrate-sensing receptors GPR41/GPR43, in human arterial stiffness needs to be determined.
“…Plasma SCFAs were measured in 200 µL and faecal SCFAs were measured from 1 g of faecal sample, all in triplicates, as previously published. 50, 51 Heptanoic acid was used as an internal standard. Samples were analysed using an Agilent GC6890 coupled to a flame-ionisation detector (FID), with helium used as the carrier gas.…”
Aims: Recent evidence supports a role for the gut microbiota in hypertension, but whether ambulatory blood pressure (BP) is associated with gut microbiota and their metabolites remains unclear. Here we characterised the function of the gut microbiota, their metabolites and receptors in untreated human hypertensive participants in metropolitan and regional areas of Australia.
Methods and Results: Ambulatory BP, faecal microbiome DNA 16S rRNA gene sequencing, plasma and faecal metabolites called short-chain fatty acid (SCFAs), and expression of their receptors were analysed in 70 untreated and otherwise healthy participants from metropolitan and regional communities. Based on machine-learning multivariate covariance analyses of de-noised amplicon sequence variant (ASV) prevalence data, we determined that there were no significant differences in gut microbiome community α- and β-diversity metrics between normotensives versus essential, white coat or masked hypertensives. However, select taxa were specific to these groups, notably Acidaminococcus spp. in essential hypertensives, and Ruminococcus spp. and Coprobacillus in normotensive subjects. Importantly, normotensive and essential hypertensive cohorts could be differentiated based on gut microbiome gene pathways and metabolites. Specifically, hypertensive participants exhibited higher plasma acetate and butyrate, but their immune cells expressed reduced levels of SCFA-activated G-protein coupled receptor 43 (GPR43).
Conclusions: While gut microbial diversity did not change in essential hypertension, there was a significant shift in microbial gene pathways, and an increase in the circulating levels of the SCFAs acetate and butyrate. Hypertensive subjects, however, had lower levels of the SCFA-sensing receptor GPR43, putatively blunting their response to BP-lowering metabolites.
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