scholarly journals P315 Short-chain fatty acid profile in inflammatory bowel disease

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S311-S312
Author(s):  
L Oliveira ◽  
L Yukie Sassaki ◽  
A Elisa Valencise Quagli ◽  
J Ribeiro de Barros
Keyword(s):  
Fatty Acid ◽  
Intestinal Inflammation ◽  
Nutrient Deficiency ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Bacterial Degradation ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
And Control ◽  
Chronic Intestinal Inflammation

Abstract Background Short-chain fatty acids (SCFAs) are products of colonic bacterial degradation of dietary fibre. They are important in the colon, affecting the morphology and function of colonocytes. SCFAs consist of a molecule with one to six carbons, of which acetate, propionate and butyrate are the most abundant. In recent decades, it has become apparent that SCFAs can play a key role in the prevention and treatment of metabolic syndrome, intestinal disorders and certain cancers. Crohn’s disease (CD) and ulcerative colitis (UC) are characterised by recurrent chronic intestinal inflammation, probably due to an inadequate immune response coupled with intestinal microbiota imbalance. The aim of this study was to evaluate the profile of SCFA in patients with UC and CD, and compared with non-ill individuals. Methods The individuals were divided into three groups: RCU, CD and control, the faeces were donated by them, and the SCFAs were measured by chromatographic analysis using a Thermo Scientific GC-MS coupled to a Thermo ISQ 230ST mass detector. All results are expressed as mean ± SEM. Results It was possible to observe a different SCFAs profile between individuals with CD and UC and control where acetate and propionate levels in patients with UC and CD were higher than in non-sick individuals and butyrate with lower levels in individuals with CD and RCU (Graph 1). SCFAs have anti-inflammatory capabilities and also a preferred energy source for colon epithelial cells, as well as lowering the pH of the colon and inhibiting the growth of pathogenic organisms. Dysbiosis decreases butyrate concentrations, which may result in nutrient deficiency at the epithelial level, altering immune responses, as well as acting directly as an anti-inflammatory agent by disabling the NFκB pathway, with a consequent decrease in inflammatory cytokine synthesis. Conclusion Thus, the reported results have implications for various physiological and pathological conditions in inflammatory bowel diseases, especially with respect to butyrate and the production of inflammatory mediators, and partly explain the beneficial effects attributed to this fatty acid in the treatment of inflammatory and inflammatory diseases support the realisation of new studies aimed at the development of therapeutic alternatives to the use of conventional anti-inflammatory drugs.

Fatty Acid Profile of Synbiotic Cheese and its Effect on Intestinal Inflammation in Rats

2019 ◽  
Vol 14 (1) ◽  
pp. 45-50
Author(s):  
Nurliyani ◽  
Harmayani Eni ◽  
Rahmatulloh Satyaguna ◽  
Rakasivi Kanita Galih Julia
Keyword(s):  
Fatty Acids ◽  
Lactic Acid ◽  
Fatty Acid ◽  
Lactic Acid Bacteria ◽  
Fatty Acid Profile ◽  
Intestinal Inflammation ◽  
Lactobacillus Rhamnosus ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Chain Fatty Acids

Porang (Amorphophallus oncophyllus) is a local perennial plant rich in glucomannan. The objective of this study was to determine the effect of porang glucomannan addition during cheese processing on fatty acid profile, organic acid and vitamin B6 of goat milk cheese ripened with Lactobacillus rhamnosus. In addition, the effect of cheese consumption on short-chain fatty acid profile in the caecum digesta of inflammatory rats was evaluated. We found that the addition of glucomannan to the cheese during its ripening increased the levels of myristic, pentadecanoic acid, and cis-oleic acids. Rats consuming this cheese had elevated cecal levels of propionic, butyric, total short-chain fatty acids, and lactic acid bacteria. Consumption of synbiotic cheese also decreased the intestinal inflammation via increasing the total lactic acid bacteria, propionic, butyric, and total short-chain fatty acids.

Effect of chronic inflammation on ileal short-chain fatty acid/bicarbonate exchange

2000 ◽  
Vol 278 (4) ◽  
pp. G585-G590 ◽  
Author(s):  
Tasos Manokas ◽  
John J. Fromkes ◽  
Uma Sundaram
Keyword(s):  
Chronic Inflammation ◽  
Intestinal Inflammation ◽  
Rabbit Model ◽  
Kinetic Studies ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Rabbit Ileum ◽  
Mechanism Of Inhibition ◽  
Chronic Intestinal Inflammation ◽  
Crypt Cells

Short-chain fatty acids (SCFA) have been demonstrated to at least partially ameliorate chronic intestinal inflammation. However, whether and how intestinal SCFA absorption may be altered during chronic intestinal inflammation is unknown. A rabbit model of chronic ileitis produced by coccidia was used to determine the effect of chronic inflammation on ileal SCFA/[Formula: see text] exchange. SCFA/[Formula: see text] exchange was present in the brush-border membrane (BBM) of villus but not crypt cells from normal rabbit ileum. An anion-exchange inhibitor, DIDS, significantly inhibited SCFA/[Formula: see text] exchange. Extravesicular Cl− did not alter the uptake of SCFA, suggesting that SCFA/[Formula: see text] exchange is a transport process distinct from Cl−/[Formula: see text] exchange. In chronically inflamed ileum, SCFA/[Formula: see text] exchange was also present only in BBM of villus cells. The exchanger was sensitive to DIDS and was unaffected by extravesicular Cl−. However, SCFA/[Formula: see text] exchange was significantly reduced in villus cell BBM vesicles (BBMV) from chronically inflamed ileum. Kinetic studies demonstrated that the maximal rate of uptake of SCFA, but not the affinity for SCFA, was reduced in chronically inflamed rabbit ileum. These data demonstrate that a distinct SCFA/[Formula: see text] exchange is present on BBMV of villus but not crypt cells in normal rabbit ileum. SCFA/[Formula: see text] exchange is inhibited in chronically inflamed rabbit ileum. The mechanism of inhibition is most likely secondary to a reduction in transporter numbers rather than altered affinity for SCFA.

Unique Regulation of Coupled NaCl Absorption by Inducible Nitric Oxide in a Spontaneous SAMP1/YitFc Mouse Model of Chronic Intestinal Inflammation

2021 ◽  
Author(s):  
Subha Arthur ◽  
Balasubramanian Palaniappan ◽  
Sheuli Afroz ◽  
Uma Sundaram
Keyword(s):  
Nitric Oxide ◽  
Intestinal Inflammation ◽  
Common Symptom ◽  
Experimental Conditions ◽  
Nacl Absorption ◽  
Samp1 Mouse ◽  
Inflammatory Bowel ◽  
And Control ◽  
Chronic Intestinal Inflammation ◽  
Inducible Nitric Oxide

Abstract In the small intestine, Na:H (NHE3) and Cl:HCO3 (DRA or PAT1) exchangers present in the brush border membrane (BBM) of absorptive villus cells are primarily responsible for the coupled absorption of NaCl, the malabsorption of which causes diarrhea, a common symptom of inflammatory bowel disease (IBD). Inducible nitric oxide (iNO), a known mediator of inflammation, is increased in the mucosa of the chronically inflamed IBD intestine. An SAMP1/YitFc (SAMP1) mouse, a spontaneous model of chronic ileitis very similar to human IBD, was used to study alterations in NaCl absorption. The SAMP1 and control AKR mice were treated with I-N(6)-(1-Iminoethyl)-lysine (L-NIL) to inhibit iNO production, and DRA/PAT1 and NHE3 activities and protein expression were studied. Though Na:H exchange activity was unaffected, Cl:HCO3 activity was significantly decreased in SAMP1 mice due to a reduction in its affinity for Cl, which was reversed by L-NIL treatment. Though DRA and PAT1 expressions were unchanged in all experimental conditions, phosphorylation studies indicated that DRA, not PAT1, is affected in SAMP1. Moreover, the altered phosphorylation levels of DRA was restored by L-NIL treatment. Inducible NO mediates the inhibition of coupled NaCl absorption by decreasing Cl:HCO3 but not Na:H exchange. Specifically, Cl:HCO3 exchanger DRA but not PAT1 is regulated at the level of its phosphorylation by iNO in the chronically inflamed intestine.

scholarly journals Association between Fecal Short-Chain Fatty Acid Levels, Diet, and Body Mass Index in Patients with Inflammatory Bowel Disease

Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 108
Author(s):  
Agnieszka Dąbek-Drobny ◽  
Olga Kaczmarczyk ◽  
Michał Woźniakiewicz ◽  
Paweł Paśko ◽  
Justyna Dobrowolska-Iwanek ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Body Mass ◽  
Intestinal Inflammation ◽  
Eating Habits ◽  
Short Chain Fatty Acids ◽  
Isobutyric Acid ◽  
Short Chain ◽  
Bacterial Metabolites ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Disturbances in the production of bacterial metabolites in the intestine have been reported in diseases associated with dysbiosis, such as inflammatory bowel diseases (IBDs) that include two conditions: Crohn disease (CD) and ulcerative colitis (UC). Short-chain fatty acids (SCFAs) are the main dietary-fiber-derived bacterial metabolites associated with the course of intestinal inflammation. In this study, we assessed the relationship between body mass index (BMI), the type of diet used, and changes in fecal SCFA levels in patients with IBD. We performed nutritional assessments using a nutritional questionnaire and determined fecal SCFA levels in 43 patients with UC, 18 patients with CD, and 16 controls. Our results revealed that subjects with a BMI > 24.99 kg/m2 had higher levels of isobutyric acid, whereas those with a BMI < 18.5 kg/m2 had lower level of butyric, isovaleric, and propionic acids. Furthermore, we observed higher levels of valeric acid in controls than in IBD patients. We did not reveal a relationship between a specific SCFA and the type of diet, but eating habits appear to be related to the observed changes in the SCFA profile depending on BMI. In conclusion, we demonstrated that BMI is associated with SCFA levels in patients with IBD.

Comparison of Bacterial Composition, Concentration, and Metabolism of Short Chain Fatty Acid in Inflammatory Bowel Disease: A Systematic Review

2021 ◽  
pp. 5978-5984
Author(s):  
David Nugraha ◽  
Natasya Ariesta Selyardi Putri ◽  
Visuddho Visuddho ◽  
Citrawati Dyah Kencono Wungu
Keyword(s):  
Systematic Review ◽  
Inflammatory Bowel Disease ◽  
Fatty Acid ◽  
Bowel Disease ◽  
Short Chain Fatty Acid ◽  
Chain Fatty Acid ◽  
Short Chain ◽  
Inflammatory Disorder ◽  
Chronic Inflammatory Disorder ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD), which consists of Crohn's disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder of the intestine. The etiology is heterogeneous and multifactorial, including genetic susceptibility, immune-mediated tissue damage, and changes of lumen microenvironment, especially short-chain fatty acid (SCFA) producing bacteria. Several studies reported a decrease in SCFA concentration in both CD and UC. In fact, SCFAs has important roles in accelerating disease remission. This systematic review aimed to evaluate the changes in SCFA concentration, the composition of SCFA-producing bacteria, and SCFA metabolism in IBD. A literature search was conducted via PubMed, Scopus, and CENTRAL by selecting studies according to inclusion and exclusion criteria. The quality and risk of bias assessment were performed using the Newcastle-Ottawa Scale (NOS). Overall, 160 UC and 127 CD patients from 5 studies were reviewed. The SCFA concentration was significantly reduced (p <0.05) in both PC and UC. Moreover, there was a decrease in major SCFA-producing bacteria. Clostridium coccoides were significantly decreased in the feces of active UC (p = 0.015) and CD (p = 0.04). Clostridium leptum was decreased on intestinal mucosal biopsy of active CD and UC (p <0.0001). Faecalibacterium prausnitzii were decreased in active CD faeces (p <0.0001) and UC (p = 0.0001). Butyrate oxidation rate was also reported to decrease in UC compared to control (p<0.0001). In conclusion, the ability of major SCFA-producing bacterial production in IBD was diminished, which implies a decreased protective and anti-inflammatory effect of SCFA that altered its metabolism.

scholarly journals Anthocyanins and intestinal barrier function: a review

2019 ◽  
Vol 5 ◽  
pp. 18-30 ◽  
Author(s):  
Jonathan C. Valdez ◽  
Bradley W. Bolling
Keyword(s):  
Barrier Function ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Berry Anthocyanins ◽  
Chronic Intestinal Inflammation

Chronic intestinal inflammation, occurring in inflammatory bowel diseases (IBD), is associated with compromised intestinal barrier function. Inflammatory cytokines disrupt tight junctions and increase paracellular permeability of luminal antigens. Thus, chronic intestinal barrier dysfunction hinders the resolution of inflammation. Dietary approaches may help mitigate intestinal barrier dysfunction and chronic inflammation. A growing body of work in rodent models of colitis has demonstrated that berry consumption inhibits chronic intestinal inflammation. Berries are a rich dietary source of polyphenolic compounds, particularly anthocyanins. However, berry anthocyanins have limited bioavailability and are extensively metabolized by the gut microbiota and host tissue. This review summarizes the literature regarding the beneficial functions of anthocyanin-rich berries in treating and preventing IBD. Here, we will establish the role of barrier function in the pathogenesis of IBD and how dietary anthocyanins and their known microbial catabolites modulate intestinal barrier function.

scholarly journals Immune system alterations in patients with inflammatory bowel disease during remission

Medicina ◽  
2008 ◽  
Vol 44 (1) ◽  
pp. 27 ◽  
Author(s):  
Jurgita Šventoraitytė ◽  
Aida Žvirblienė ◽  
Gediminas Kiudelis ◽  
Rimantas Žalinkevičius ◽  
Aurelija Žvirblienė ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Bowel Disease ◽  
Immune Homeostasis ◽  
Th2 Cytokines ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
And Control

Objective. Perturbed immune homeostasis elicited by misbalanced production of proinflammatory and anti-inflammatory cytokines is characteristic of inflammatory bowel disease. The aim of this study was to evaluate cytokine profile in patients with different forms of inflammatory bowel disease – ulcerative colitis and Crohn’s disease – during clinical remission phase. Material and methods. Production of proinflammatory Th1 cytokines (tumor necrosis factoralpha (TNF-a), interferon-gamma (IFN-g)) and anti-inflammatory Th2 cytokines (interleukin- 10 (IL-10) and interleukin-13 (IL-13)) was analyzed in peripheral blood mononuclear cells of patients with inflammatory bowel disease (9 with ulcerative colitis and 9 with Crohn’s disease) and control subjects (n=11) by enzyme-linked immunosorbent assay (two-site ELISA). Results. The results of the study revealed that the level of TNF-a after stimulation with phytohemagglutinin in patients with Crohn’s disease was significantly higher in comparison to both patients with ulcerative colitis and controls (P<0.001 and P<0.01, respectively). The secretion of IFN-g both in patients with Crohn’s disease and ulcerative colitis was lower than that in controls (P=0.05 and P<0.01, respectively), but it normalized after stimulation with phytohemagglutinin. The levels of IL-10 and IL-13 were significantly (P<0.01) higher in patients with Crohn’s disease than in patients with ulcerative colitis and control group before and after stimulation with phytohemagglutinin. Conclusions. The results of our study provide evidence that in patients with inflammatory bowel disease, the imbalance between production of proinflammatory Th1 and anti-inflammatory Th2 cytokines persists even during remission of the disease, and disturbances of immune homeostasis are significantly more expressed in patients with Crohn’s disease than in patients with ulcerative colitis.

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