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Does intestinal dysbiosis contribute to an aberrant inflammatory response to severe acute respiratory syndrome coronavirus 2 in frail patients?
Terruzzi, I, Senesi, P
Nutrition (Burbank, Los Angeles County, Calif.). 2020;:110996
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Abstract
In a few months, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has become the main health problem worldwide. Epidemiologic studies revealed that populations have different vulnerabilities to SARS-CoV-2. Severe outcomes of the coronavirus disease 2019 (COVID-19) with an increased risk of death are observed in patients with metabolic syndrome, as well as diabetic and heart conditions (frail population). Excessive proinflammatory cytokine storm could be the main cause of increased vulnerability in this frail population. In patients with diabetes and/or heart disease, a low inflammatory state is often associated with gut dysbiosis. The increase amount of microbial metabolites (i.e., trimethylamine N-oxide and lipopolysaccharide), which generate an inflammatory microenvironment, is probably associated with an improved risk of severe illness from COVID-19. Nutritional interventions aimed at restoring the gut microbial balance could represent preventive strategies to protect the frail population from COVID-19. This narrative review presents the possible molecular mechanisms by which intestinal dysbiosis that enhances the inflammatory state could promote the spread of SARS-CoV-2 infection. Some nutritional strategies to counteract inflammation in frail patients are also analyzed.
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From the intestinal flora to the microbiome.
Sebastián Domingo, JJ, Sánchez Sánchez, C
Revista espanola de enfermedades digestivas. 2018;(1):51-56
Abstract
In this article, the history of the microbiota is reviewed and the related concepts of the microbiota, microbiome, metagenome, pathobiont, dysbiosis, holobiont, phylotype and enterotype are defined. The most precise and current knowledge about the microbiota is presented and the metabolic, nutritional and immunomodulatory functions are reviewed. Some gastrointestinal diseases whose pathogenesis is associated with the intestinal microbiota, including inflammatory bowel disease, irritable bowel syndrome and celiac disease, among others, are briefly discussed. Finally, some prominent and promising data with regard to the fecal microbiota transplantation in certain digestive illness are discussed.
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The Effect of Extended Release Niacin on Markers of Mineral Metabolism in CKD.
Malhotra, R, Katz, R, Hoofnagle, A, Bostom, A, Rifkin, DE, Mcbride, R, Probstfield, J, Block, G, Ix, JH
Clinical journal of the American Society of Nephrology : CJASN. 2018;(1):36-44
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Abstract
BACKGROUND AND OBJECTIVES Niacin downregulates intestinal sodium-dependent phosphate transporter 2b expression and reduces intestinal phosphate transport. Short-term studies have suggested that niacin lowers serum phosphate concentrations in patients with CKD and ESRD. However, the long-term effects of niacin on serum phosphate and other mineral markers are unknown. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS The Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Trial was a randomized, double-blind, placebo-controlled trial testing extended release niacin in persons with prevalent cardiovascular disease. We examined the effect of randomized treatment with niacin (1500 or 2000 mg) or placebo on temporal changes in markers of mineral metabolism in 352 participants with eGFR<60 ml/min per 1.73 m2 over 3 years. Changes in each marker were compared over time between the niacin and placebo arms using linear mixed effects models. RESULTS Randomization to niacin led to 0.08 mg/dl lower plasma phosphate concentrations per year of treatment compared with placebo (P<0.01) and 0.25 mg/dl lower mean phosphate 3 years after baseline (3.32 versus 3.57 mg/dl; P=0.03). In contrast, randomization to niacin was not associated with statistically significant changes in plasma intact fibroblast growth factor 23, parathyroid hormone, calcium, or vitamin D metabolites over 3 years. CONCLUSIONS The use of niacin over 3 years lowered serum phosphorous concentrations but did not affect other markers of mineral metabolism in participants with CKD.
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Regulatory efficacy of fermented plant extract on the intestinal microflora and lipid profile in mildly hypercholesterolemic individuals.
Chiu, HF, Chen, YJ, Lu, YY, Han, YC, Shen, YC, Venkatakrishnan, K, Wang, CK
Journal of food and drug analysis. 2017;(4):819-827
Abstract
In recent years, the use of fermented plant products to protect against various metabolic syndromes has been increasing enormously. The objective of this study was to check the regulatory efficacy of fermented plant extract (FPE) on intestinal microflora, lipid profile, and antioxidant status in mildly hypercholesterolemic volunteers. Forty-four mildly hypercholesterolemic individuals (cholesterol 180-220 mg/dL) were recruited and assigned to two groups: experimental or placebo. Volunteers were requested to drink either 60 mL of FPE or placebo for 8 weeks. Anthropometric measurements were done in the initial, 4th, 8th, and 10th weeks. The anthropometric parameters such as body weight, body fat, and body mass index were markedly lowered (p<0.05) on FPE intervention participants. Moreover, the total antioxidant capacity and total phenolics in plasma were considerably increased along with a reduction (p<0.05) in total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-c) after FPE supplementation. Participants who drank FPE showed a pronounced increase (p<0.05) in the number of beneficial bacteria such as Bifidobacterium spp. and Lactobacillus spp., whereas the number of harmful bacteria such as Escherichia coli and Clostridium perfringens (p<0.05) were concomitantly reduced. Furthermore, the lag time of LDL oxidation was substantially ameliorated in FPE-administered group, thus indicating its antioxidative and cardioprotective properties. Treatment with FPE substantially improved the intestinal microflora and thereby positively regulated various physiological functions by lowering the anthropometric parameters, TC, and LDL-c, and remarkably elevated the antioxidant capacity and lag time of LDL oxidation. Therefore, we recommended FPE beverage for combating hypercholesterolemia.
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Visceral Congestion in Heart Failure: Right Ventricular Dysfunction, Splanchnic Hemodynamics, and the Intestinal Microenvironment.
Polsinelli, VB, Sinha, A, Shah, SJ
Current heart failure reports. 2017;(6):519-528
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Abstract
PURPOSE OF REVIEW Visceral venous congestion of the gut may play a key role in the pathogenesis of right-sided heart failure (HF) and cardiorenal syndromes. Here, we review the role of right ventricular (RV) dysfunction, visceral congestion, splanchnic hemodynamics, and the intestinal microenvironment in the setting of right-sided HF. We review recent literature on this topic, outline possible mechanisms of disease pathogenesis, and discuss potential therapeutics. RECENT FINDINGS There are several mechanisms linking RV-gut interactions via visceral venous congestion which could result in (1) hypoxia and acidosis in enterocytes, which may lead to enhanced sodium-hydrogen exchanger 3 (NHE3) expression with increased sodium and fluid retention; (2) decreased luminal pH in the intestines, which could lead to alteration of the gut microbiome which could increase gut permeability and inflammation; (3) alteration of renal hemodynamics with triggering of the cardiorenal syndrome; and (4) altered phosphate metabolism resulting in increased pulmonary artery stiffening, thereby increasing RV afterload. A wide variety of therapeutic interventions that act on the RV, pulmonary vasculature, intestinal microenvironment, and the kidney could alter these pathways and should be tested in patients with right-sided HF. The RV-gut axis is an important aspect of HF pathogenesis that deserves more attention. Modulation of the pathways interconnecting the right heart, visceral congestion, and the intestinal microenvironment could be a novel avenue of intervention for right-sided HF.
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[Physiological patterns of intestinal microbiota. The role of dysbacteriosis in obesity, insulin resistance, diabetes and metabolic syndrome].
Halmos, T, Suba, I
Orvosi hetilap. 2016;(1):13-22
Abstract
The intestinal microbiota is well-known for a long time, but due to newly recognized functions, clinician's attention has turned to it again in the last decade. About 100 000 billion bacteria are present in the human intestines. The composition of bacteriota living in diverse parts of the intestinal tract is variable according to age, body weight, geological site, and diet as well. Normal bacteriota defend the organism against the penetration of harmful microorganisms, and has many other functions in the gut wall integrity, innate immunity, insulin sensitivity, metabolism, and it is in cross-talk with the brain functions as well. It's a recent recognition, that intestinal microbiota has a direct effect on the brain, and the brain also influences the microbiota. This two-way gut-brain axis consists of microbiota, immune and neuroendocrine system, as well as of the autonomic and central nervous system. Emerging from fermentation of carbohydrates, short-chain fatty acids develop into the intestines, which produce butyrates, acetates and propionates, having favorable effects on different metabolic processes. Composition of the intestinal microbiota is affected by the circadian rhythm, such as in shift workers. Dysruption of circadian rhythm may influence intestinal microbiota. The imbalance between the microbiota and host organism leads to dysbacteriosis. From the membrane of Gram-negative bacteria lipopolysacharides penetrate into the blood stream, via impaired permeability of the intestinal mucosa. These processes induce metabolic endotoxaemia, inflammation, impaired glucose metabolism, insulin resistance, obesity, and contribute to the development of metabolic syndrome, type 2 diabetes, inflammarory bowel diseases, autoimmunity and carcinogenesis. Encouraging therapeutic possibility is to restore the normal microbiota either using pro- or prebiotics, fecal transplantation or bariatric surgery. Human investigations seem to prove that fecal transplant from lean healthy individuals into obese diabetic patients improved all the pathological parameters. Wide spread use of bariatric surgery altered gut microbiota and improved metabolic parameters apart from surgery itself. Pathomechanism is not yet completely clarified. Clinicians hope, that deeper understanding of complex functions of intestinal microbiota will contribute to develop more effective therapeutic proceedings against diabetes, metabolic syndrome, and obesity.
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Fine-tuning of the mucosal barrier and metabolic systems using the diet-microbial metabolite axis.
Nagai, M, Obata, Y, Takahashi, D, Hase, K
International immunopharmacology. 2016;:79-86
Abstract
The human intestinal microbiota has profound effects on human physiology, including the development and maintenance of the host immune and metabolic systems. Under physiological conditions, the intestinal microbiota maintains a symbiotic relationship with the host. Abnormalities in the host-microbe relationship, however, have been implicated in multiple disorders such as inflammatory bowel diseases (IBDs), metabolic syndrome, and autoimmune diseases. There is a close correlation between dietary factors and the microbial composition in the gut. Long-term dietary habits influence the composition of the gut microbial community and consequently alter microbial metabolic activity. The diet-microbiota axis plays a vital role in the regulation of the host immune system, at least partly through altering microbial metabolism. In this review, we will describe the current findings regarding how dietary factors and microbial metabolites regulate the host immune system.
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[The microbiome of the gut in critically ill patients].
Salzberger, B, Rauscher, C
Medizinische Klinik, Intensivmedizin und Notfallmedizin. 2015;(7):521-5
Abstract
BACKGROUND The complexity and diversity of the human intestinal microbiome has only recently been characterized. The multiple metabolic and immunologic effects of the bacterial flora have demonstrated the symbiosis between the microbiome and its host. This symbiosis is disturbed in a multitude of diseases, especially in critically ill patients. OBJECTIVES A review of the changes in the intestinal microbiome of critically ill patients and the use of probiotics. MATERIAL AND METHODS Nonsystematic literature search in PubMed on the topics: (1) changes in the intestinal microbiome in critically ill patients, (2) interventions using probiotics in critically ill patients, and (3) use of fecal transplantation in Clostridium difficile colitis. RESULTS Trauma, sepsis, systemic inflammatory response syndrome, and other conditions lead to shifts in the composition of the intestinal microbiome, which are correlated with clinical outcome. The most obvious change is a profound loss of obligate anaerobe bacteria, leading also to metabolic changes. Probiotics have been used in several studies and show efficacy in the reduction of infectious complication but not in overall mortality. C. difficile colitis as the model disease for a disturbed microbiome can be treated effectively by transfer of donor feces, which also restores the diversity of the microbiome. CONCLUSION Taking into account the successful intervention of fecal transplantation on the intestinal microbiome, new products developed using the current knowledge of the intestinal microbiome could be more effective.
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Gut microbiota and non-alcoholic fatty liver disease.
Gkolfakis, P, Dimitriadis, G, Triantafyllou, K
Hepatobiliary & pancreatic diseases international : HBPD INT. 2015;(6):572-81
Abstract
BACKGROUND Non-alcoholic fatty liver disease (NAFLD) is a common disorder with poorly understood pathogenesis. Beyond environmental and genetic factors, cumulative data support the causative role of gut microbiota in disease development and progression. DATA SOURCE We performed a PubMed literature search with the following key words: "non-alcoholic fatty liver disease", "non-alcoholic steatohepatitis", "fatty liver", "gut microbiota" and "microbiome", to review the data implicating gut microbiota in NAFLD development and progression. RESULTS Recent metagenomic studies revealed differences in the phylum and genus levels between patients with fatty liver and healthy controls. While bacteroidetes and firmicutes remain the dominant phyla among NAFLD patients, their proportional abundance and genera detection vary among different studies. New techniques indicate a correlation between the methanogenic archaeon (methanobrevibacter smithii) and obesity, while the bacterium akkermanshia municiphila protects against metabolic syndrome. Among NAFLD patients, small intestinal bacterial overgrowth detected by breath tests might induce gut microbiota and host interactions, facilitating disease development. CONCLUSIONS There is evidence that gut microbiota participates in NAFLD development through, among others, obesity induction, endogenous ethanol production, inflammatory response triggering and alterations in choline metabolism. Further studies with emerging techniques are needed to further elucidate the microbiome and host crosstalk in NAFLD pathogenesis.
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Serotonergic reinforcement of intestinal barrier function is impaired in irritable bowel syndrome.
Keszthelyi, D, Troost, FJ, Jonkers, DM, van Eijk, HM, Lindsey, PJ, Dekker, J, Buurman, WA, Masclee, AA
Alimentary pharmacology & therapeutics. 2014;(4):392-402
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Abstract
BACKGROUND Alterations in serotonergic (5-HT) metabolism and/or intestinal integrity have been associated with irritable bowel syndrome (IBS). AIMS To assess the effects of the precursor of 5-HT, 5-hydroxytryptophan (5-HTP), on mucosal 5-HT availability and intestinal integrity, and to assess potential differences between healthy controls and IBS patients. METHODS Fifteen IBS patients and 15 healthy volunteers participated in this randomised double-blind placebo-controlled study. Intestinal integrity was assessed by dual-sugar test and by determining the mucosal expression of tight junction proteins after ingestion of an oral bolus of 100 mg 5-HTP or placebo. Mucosal serotonergic metabolism was assessed in duodenal biopsy samples. RESULTS 5-HTP administration significantly increased mucosal levels of 5-HIAA, the main metabolite of 5-HT, in both healthy controls (7.1 ± 1.7 vs. 2.5 ± 0.7 pmol/mg, 5-HTP vs. placebo, P = 0.02) and IBS patients (20.0 ± 4.8 vs. 8.1 ± 1.3 pmol/mg, 5-HTP vs. placebo, P = 0.02), with the latter group showing a significantly larger increase. Lactulose/L-rhamnose ratios were significantly lower after administration of 5-HTP (P < 0.05) in healthy controls and were accompanied by redistribution of zonula occludens-1 (ZO-1), pointing to reinforcement of the barrier. In IBS, expression of the tight junction proteins was significantly lower compared to healthy controls, and 5-HTP resulted in a further decrease in occludin expression. CONCLUSIONS Oral 5-HTP induced alterations in mucosal 5-HT metabolism. In healthy controls, a reinforcement of the intestinal barrier was seen whereas such reaction was absent in IBS patients. This could indicate the presence of a serotonin-mediated mechanism aimed to reinforce intestinal barrier function, which seems to dysfunction in IBS patients.