The Impact of Dietary Fiber on Gut Microbiota in Host Health and Disease

Cell Host & Microbe, Journal Year: 2018, Volume and Issue: 23(6), P. 705 - 715

Published: June 1, 2018

Language: Английский

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The intestinal microbiota fuelling metabolic inflammation

Nature reviews. Immunology, Journal Year: 2019, Volume and Issue: 20(1), P. 40 - 54

Published: Aug. 6, 2019

Language: Английский

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Gut Microbiota and Short Chain Fatty Acids: Implications in Glucose Homeostasis

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(3), P. 1105 - 1105

Published: Jan. 20, 2022

Gut microbiota encompasses a wide variety of commensal microorganisms consisting trillions bacteria, fungi, and viruses. This microbial population coexists in symbiosis with the host, related metabolites have profound effects on human health. In this respect, gut plays pivotal role regulation metabolic, endocrine, immune functions. Bacterial include short chain fatty acids (SCFAs) acetate (C2), propionate (C3), butyrate (C4), which are most abundant SCFAs body anions colon. made from fermentation dietary fiber resistant starch gut. They modulate several metabolic pathways involved obesity, insulin resistance, type 2 diabetes. Thus, diet might influence composition activity, production, effects. narrative review, we discuss relevant research focusing relationship between microbiota, SCFAs, glucose metabolism.

Language: Английский

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NAFLD and cardiovascular diseases: a clinical review

Clinical Research in Cardiology, Journal Year: 2020, Volume and Issue: 110(7), P. 921 - 937

Published: July 21, 2020

Abstract Non-alcoholic fatty liver DISEASE (NAFLD) is the most common chronic disease in Western countries and affects approximately 25% of adult population. Since NAFLD frequently associated with further metabolic comorbidities such as obesity, type 2 diabetes mellitus, or dyslipidemia, it generally considered hepatic manifestation syndrome. In addition to its potential cause liver-related morbidity mortality, also subclinical clinical cardiovascular (CVD). Growing evidence indicates that patients are at substantial risk for development hypertension, coronary heart disease, cardiomyopathy, cardiac arrhythmias, which clinically result increased mortality. The natural history variable vast majority will not progress from simple steatosis fibrosis end stage disease. However, progressive forms NAFLD, including non-alcoholic steatohepatitis (NASH) and/or advanced fibrosis, well concomitant types highest CVD. This review describes underlying pathophysiological mechanisms linking CVD, discusses role a dysfunction factor, focuses on manifestations patients.

Language: Английский

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Gut Microbiota as a Trigger for Metabolic Inflammation in Obesity and Type 2 Diabetes

Frontiers in Immunology, Journal Year: 2020, Volume and Issue: 11

Published: Oct. 16, 2020

The gut microbiota has been linked to the development of obesity and type 2 diabetes (T2D). underlying mechanisms as how intestinal may contribute T2D are only partly understood. It becomes progressively clear that is characterized by a chronic state low-grade inflammation, which insulin resistance. Here, we review current evidence microbiota, metabolites they produce, could drive resistance in T2D, possibly initiating an inflammatory response. First, will summarize major findings about immunological microbial changes these metabolic diseases. Next, give detailed view on have implicated inflammation. Lastly, critically discuss clinical studies focus interaction between immune system disease. Overall, there strong tripartite host metabolism critical partaker pathophysiology T2D.

Language: Английский

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Ketogenic Diets Alter the Gut Microbiome Resulting in Decreased Intestinal Th17 Cells

Cell, Journal Year: 2020, Volume and Issue: 181(6), P. 1263 - 1275.e16

Published: May 20, 2020

Language: Английский

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Dysregulated lipid metabolism links NAFLD to cardiovascular disease

Molecular Metabolism, Journal Year: 2020, Volume and Issue: 42, P. 101092 - 101092

Published: Oct. 1, 2020

Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming a global health problem. Cardiovascular diseases (CVD) are the most common cause of mortality in NAFLD patients. and CVD share several risk factors including obesity, insulin resistance, type 2 diabetes (T2D). Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense low-density lipoprotein (LDL) particles, decreased high-density cholesterol (HDL-C) levels, often observed patients.In this review, we highlight recent epidemiological studies evaluating link between risk. We further focus on mechanistic insights into links altered metabolism. also discuss current therapeutic strategies for their potential impact NAFLD-associated risk.Alterations hepatic lipid metabolism major contributing to patients, many promising NASH therapies development improve dyslipidemia clinical trials.

Language: Английский

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You Are What You Eat—The Relationship between Diet, Microbiota, and Metabolic Disorders—A Review

Nutrients, Journal Year: 2020, Volume and Issue: 12(4), P. 1096 - 1096

Published: April 15, 2020

The gut microbiota (GM) is defined as the community of microorganisms (bacteria, archaea, fungi, viruses) colonizing gastrointestinal tract. GM regulates various metabolic pathways in host, including those involved energy homeostasis, glucose and lipid metabolism, bile acid metabolism. relationship between alterations intestinal diseases associated with civilization well documented. dysbiosis pathogenesis diverse diseases, such syndrome, cardiovascular celiac disease, inflammatory bowel neurological disorders. Multiple factors modulate composition how it physically functions, but one major triggering establishment diet. In this paper, we reviewed current knowledge about nutrition, microbiota, host status. We described macronutrients (proteins, carbohydrates, fat) different dietary patterns (e.g., Western-style diet, vegetarian Mediterranean diet) interact activity GM, bacterial has an influence on disorders, obesity, type 2 diabetes, hyperlipidemia.

Language: Английский

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Multiple Parallel Hits Hypothesis in Nonalcoholic Fatty Liver Disease: Revisited After a Decade

Hepatology, Journal Year: 2020, Volume and Issue: 73(2), P. 833 - 842

Published: Aug. 12, 2020

Nonalcoholic fatty liver disease (NAFLD) is an epidemic disease, affecting approximately one quarter of the entire population in world.(1) This encompasses a broad spectrum clinical phenotypes ranging from hepatic steatosis to nonalcoholic steatohepatitis (NASH), fibrotic NASH, advanced fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Although inflammation NAFLD appears less prognostically relevant when compared fibrosis,(2) latter may be cumulative result former.(3) Noninvasive assessment fibrosis (e.g., by transient elastography) has reduced need for invasive procedures such as biopsy,(4) although late-stage trials still require histologic endpoints. The plays crucial role glucose lipid metabolism. frequently present obesity reflects risk factor many metabolic diseases type 2 diabetes (T2D).(5) In turn, T2D associated with up 90% patients. been linked various extrahepatic disorders cardiovascular complications(6) chronic kidney disease.(7) Furthermore, not only major HCC but also increased rate malignancies gastrointestinal gynecological malignancies.(4) cancer seems even higher than itself.(8) As such, prototypic systemic disorder targeting organs throughout body. pathophysiology underlying this complex incompletely understood. A decade ago, we proposed multiple parallel hits hypothesis which lipotoxicity adipose tissue (AT) alterations gut microbial functions contribute evolution NAFLD.(9) Progress over last was substantial that AT inflammation(10) microbiome (and related metabolites) evolved players pathogenesis NAFLD.(11, 12) dietary components other proinflammatory potential have identified. Finally, genetic pathways play manifestation; several hits, patatin-like phospholipase domain containing 3, transmembrane 6 superfamily member 2, glucokinase regulator, membrane-bound O-acyltransferase 7, hydroxysteroid 17-beta dehydrogenase 13, are involved especially metabolism.(13) review, will discuss pathophysiological factors focusing on intricate triangular interplay between tract, AT, liver. Normal composed adipocytes, fibroblasts, endothelial cells, resident macrophages cells immune system collectively regulate host metabolism energy storage.(14) White depots comprise visceral (VAT) subcutaneous (SAT), which, together liver, participate acid health, communicates control homeostasis.(15) obesity, characterized cytokine chemokine expression infiltration example, leukocytes, serve fuel local inflammation. inflammatory state contributes inflammation, deteriorate insulin resistance, exemplifying aspects AT–liver axis.(9, 10) hallmarks influx macrophages, cluster differentiation 4–positive (CD4+) CD8+ T dendritic natural killer (NK) cytokines/chemokines.(16) Primary cues remain poorly explored arguably involve diet-induced stress subsequently induces response cell infiltration. initial fueled self-maintained tissue-infiltrating cells. For recruitment (ATMs) dependent chemokines C-C motif ligand (CCL2), expressed obese animals patients.(17) Adaptive immunity cells) recruited antigen-presenting precedes ATM accumulation.(18) Expression (besides CCL2) CCL5 (also known regulated upon activation, normal expressed, secreted) or CCL13 patients.(19) Importantly, most these cytokines tumor necrosis alpha (TNFα), interleukin 1-beta (IL-1β), IL-6. TNFα first described adipokine obesity-related resistance murine models, its human obesity.(20) Similarly, preclinical evidence indicated key IL-1β IL-1α-deficient, IL-1β-deficient, 1 IL-1 receptor–deficient mice protected against high-fat diet–induced resistance(21); expression.(22) IL-37, anti-inflammatory family member, highly subjects able improve experimental models.(23, 24) IL-6 produced mostly ATMs adipocytes.(25) importance SAT source circulating convincingly demonstrated, 15%-35% being derived tissue.(26) Both VAT produce large amounts disorders, both sources biologically affect sensitivity.(27) We investigated morbidly patients undergoing bariatric surgery. TNFα, IL-1β, IL-6, strongly after successful weight loss.(23, 28) adiponectin leptin (prototypic immunomodulatory adipokines) critically disorders.(29) Collectively, studies highlight cellular, cytokine, adipokine. networks (see Fig. 1). Clinical provide cellular molecular correlate degree disease. Du Plessis colleagues studied transcriptomic profiles VAT, functional characteristics ATMs, severity 113 surgery.(30) They found genes comparing NASH. NASH exhibited number CD11c+CD206+ (C-C motif) receptor–positive accompanied release chemokines. Most importantly, directly correlated inflammation.(30) study investigating 3,197 participants observed independently obesity.(31) no proof concept NAFLD, they clearly link light (mechanistic) report axis disorders. Insulin hallmark NAFLD,(32) occurs tissues muscle, AT.(33) While it commonly conceived emerges consequent recent demonstrated through monocyte chemoattractant protein 1–regulated leukocyte recruitment.(34) These findings interesting accelerates lipolysis mitogen-activated kinase (MAPK) signaling, results activation ß3-adrenergic receptor.(35) Lipolysis enhanced free export promoting potentially NAFLD. line this, correlates (especially fibrosis); improvement pioglitazone, peroxisome proliferator–activated receptor-gamma agonist, resulted decrease hepatocyte ballooning patients.(36) Indeed, NAFLD.(37) study, authors established macrophage measuring soluble CD183, proposing acids might involved. support crosstalk aforementioned notable, descriptive can indirect mammals. Bijnen transplanted lean, obese, ATM-depleted lean Ldr−/− mice.(38) transplantation injury pronounced AT. Liver paralleled numbers neutrophils, effect mainly attributed synthesis neutrophil chemotaxis proteins (C-X-C ligands 14 16 ATM.(38) previously hypothesized tissue-specific knockout (KO) models AT-specific KO mice) would reveal numerous reported took advantage adipocyte-specific mouse models; few discussed here. deletion receptor and/or insulin-like growth severe lipodystrophy progressive resembling dysplastic nodules at week 52.(39) Lipid peroxidation critical mechanism model.(39) deficiency hormone-sensitive lipase causes increase lipodystrophy, impaired synthesis, resistance.(40) contrast, lipoprotein angiopoietin-like 4 (which controls metabolism) attenuates steatosis, atherosclerosis.(41) shown I interferon worsens perturbation, gain, intolerance.(42) However, did impact our model. indicate specific hubs deserve dissected more detail. Various impinge gut–liver axis. shaped metabolites hormones system.(43) section made deciphering intestinal microbiota identification NASH-associated signature,(44) preceded smaller NAFLD.(45) abundance Proteobacteria, Enterobacteriaceae, Escherichia coli differed microbiomes(45); association Bacteroidetes simple healthy controls.(46) Boursier histology-proven 57 patients.(47) Bacteroides depending while Prevotella decreased. convincing example signature comes Loomba colleagues.(44) 86 histologically defined identified 37 bacterial species, allowed them distinguish mild versus fibrosis. Advanced Proteobacteria Firmicutes Faecalibacterium prausnitzii. Such prevalent case cirrhosis.(48) An important bacteria-derived endotoxin disease-contributing had claimed already 20 years ago.(49) confirmed presence livers. Patients concentrations similar accumulation hepatocytes, toll-like macrophages.(50) Further intrahepatic another reporting portal tract.(51) Experimental endotoxin-producing strains Enterobacter cloacae B29, PY102, Klebsiella pneumoniae A7 promoted germ-free diet.(52) Moreover, ethanol-producing isolated caused oral gavaging.(53) Due space constraints, do barrier NAFLD.(54) Vice versa, modulate susceptibility excellently reviewed recently(55) conclusion, overwhelming underpins very exciting rapidly evolving topic (i.e., AT) blood) expands beyond dysbiosis Bacterial 16S ribosomal DNA indeed detected blood, diabetes,(56) blood NAFLD.(57) tissue, material taxa two cohorts NAFLD.(51) Sookoian colleagues(51) severely (similar microbiome). different including solid cancers,(58) T2D, obesity.(59) reminiscent omental, SAT, subjects.(60) Schierwagen central, hepatic, venous peripheral cirrhosis receiving transjugular portosystemic shunt(61); some bacteria could cultivated sites. and, cases, live circulation diseased liver/AT. implications health describe compelling window opportunity research were considered sterile. Metagenomic sequencing metabolite screens (metabolomics) allow insight into repertoire communities. metabolomics recently.(12) Hoyles plasma urine metabolome, fecal metagenome bacteria), transcriptome transcriptional profile) women.(62) phenylacetate) steatosis. Fecal transfer women high-grade feeding phenylacetate mice.(62) search vein dysfunction, Koh discovered imidazole propionate, microbially histidine-derived metabolite.(63) metabolite, propionate affected signaling p38 MAPK phosphorylation p62, finally mechanistic target rapamycin.(63) Levels N,N,N-trimethyl-5-aminovaleric acid, bacteria, serum NAFLD; deteriorated steatosis.(64) Other 3-(4-hydroxphenyl)lactate discriminated without unknown.(65) combination 10 showed powerful discriminatory effects detecting greater diagnostic accuracy Fibrosis-4 index.(66) increasingly recognized intestine, Future fascinating insights bears therapeutic) use. Besides pathways, interactions. Colonic sensitivity under diet.(67) By generating macrophage-specific epithelium–specific mice, decreased colonic permeability, improved tolerance, highlighting gut–AT axis.(67) Interestingly, products commensal L-lactate acetate enterocyte altered storage oxidation.(68) distal effects, influencing lipid-driven atherosclerosis Many exert development NAFLD.(69) Dietary metabolism(70) act microbiome, referred "dysbiosis."(71) so far damage Western diet high fat consumption intake alcohol, salt, refrained grains, fructose, red processed meat developing progressing NAFLD.(69, 72) volunteers endotoxemia low-grade inflammation.(73) Trans-fatty unsaturated vegetables enriched snack foods, fried margarines. Intake trans-fat negatively all-cause mortality coronary heart mortality.(74) well studied. Trans-fat single function tests index.(75) Preclinical data propose trans-fats promote cholesterogenesis,(76) trans-fat-induced if trans-fatty deleted pool, exact mechanisms elusive.(77) Fructose fibrosis.(78) triggers de novo lipogenesis process involves microbiota-derived acetate.(79) subjects, however, excess isocaloric fructose 8 weeks detrimental liver.(80) raises doubts whether damages Wheat amylase trypsin inhibitors, common wheat component, activates macrophages(81) aggravates inflammation.(82) converts nutrients choline carnitine trimethylamine, metabolized flavin monooxygenases trimethylamine N-oxide (TMAO),(83) discontinuation TMAO levels within weeks.(84) Numerous diseases.(85) relationship trial 60 biopsy-proven lower betaine betaine/choline ratio.(86) Administration diet, involving bile farnesoid X antagonism.(87) Therefore, food thereby initiate processes outside tract. oppose above-described pool metabolites. indole, tryptophan derivate microbiota, improves mice; low NAFLD.(88) interventional using either low-sugar diet,(89) carbohydrate-restricted diet,(90) Mediterranean diet(91) beneficial defined. intervention promising strategy treat future.(69) decade, tract emerged drivers Despite fact pathogenesis, randomized controlled specifically lacking. Altered involving, NAFLD.(92) Interactions bidirectional, experiments transgenic exemplified plethora define loss behind metabolism.(33, 54, 93) corroborated 2010 hypothesis,(9) forming based gained animal trials. better understanding translation novel therapeutics endemic gratefully acknowledge Austrian Federal Ministry Science, Research, Economy National Foundation Technology, Development. All contributions discussion content wrote, edited article.

Language: Английский

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Dietary Fructose and the Metabolic Syndrome

Nutrients, Journal Year: 2019, Volume and Issue: 11(9), P. 1987 - 1987

Published: Aug. 22, 2019

Abstract: Consumption of fructose, the sweetest all naturally occurring carbohydrates, has increased dramatically in last 40 years and is today commonly used commercially soft drinks, juice, baked goods. These products comprise a large proportion modern diet, particular children, adolescents, young adults. A body evidence associate consumption fructose other sugar-sweetened beverages with insulin resistance, intrahepatic lipid accumulation, hypertriglyceridemia. In long term, these risk factors may contribute to development type 2 diabetes cardiovascular diseases. Fructose absorbed small intestine metabolized liver where it stimulates fructolysis, glycolysis, lipogenesis, glucose production. This result hypertriglyceridemia fatty liver. Therefore, understanding mechanisms underlying intestinal hepatic metabolism important. Here we review recent linking excessive health markers components Metabolic Syndrome.

Language: Английский

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