Physical data
\r\n\t
",isbn:"978-1-83969-561-2",printIsbn:"978-1-83969-560-5",pdfIsbn:"978-1-83969-562-9",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"65f2a1fef9c804c29b18ef3ac4a35066",bookSignature:"Dr. Luis Loures",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10756.jpg",keywords:"Urban Processes, Urban Patterns, Redevelopment Strategies, Landscape, Land Transformation, Urban Models, Urban Evolution, Urban Organisation, Legislation, Sustainable Development, Green Infrastructure, Regional Planning",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"February 23rd 2021",dateEndSecondStepPublish:"March 22nd 2021",dateEndThirdStepPublish:"May 21st 2021",dateEndFourthStepPublish:"August 9th 2021",dateEndFifthStepPublish:"October 8th 2021",remainingDaysToSecondStep:"a month",secondStepPassed:!0,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"Dr. Loures has worked on pioneering research on circular planning applied to post-industrial landscape redevelopment. Since he graduated he has published several peer-reviewed papers at the national and international levels and he has been a guest researcher and lecturer both at Michigan State University (USA) and at the University of Toronto (Canada) where he has developed part of his Ph.D. research with the Financial support from the Portuguese Foundation for Science and Technology (Ph.D. grant).",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"108118",title:"Dr.",name:"Luis",middleName:null,surname:"Loures",slug:"luis-loures",fullName:"Luis Loures",profilePictureURL:"https://mts.intechopen.com/storage/users/108118/images/system/108118.png",biography:"Luís Loures is a Landscape Architect and Agronomic Engineer, Vice-President of the Polytechnic Institute of Portalegre, who holds a Ph.D. in Planning and a Post-Doc in Agronomy. Since he graduated, he has published several peer reviewed papers at the national and international levels and he has been a guest researcher and lecturer both at Michigan State University (USA), and at University of Toronto (Canada) where he has developed part of his Ph.D. research with the Financial support from the Portuguese Foundation for Science and Technology (Ph.D. grant).\nDuring his academic career he had taught in several courses in different Universities around the world, mainly regarding the fields of landscape architecture, urban and environmental planning and sustainability. Currently, he is a researcher both at VALORIZA - Research Centre for Endogenous Resource Valorization – Polytechnic Institute of Portalegre, and the CinTurs - Research Centre for Tourism, Sustainability and Well-being, University of Algarve where he is a researcher on several financed research projects focusing several different investigation domains such as urban planning, landscape reclamation and urban redevelopment, and the use of urban planning as a tool for achieving sustainable development.",institutionString:"Polytechnic Institute of Portalegre",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"8",totalChapterViews:"0",totalEditedBooks:"2",institution:{name:"Polytechnic Institute of Portalegre",institutionURL:null,country:{name:"Portugal"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"10",title:"Earth and Planetary Sciences",slug:"earth-and-planetary-sciences"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"205697",firstName:"Kristina",lastName:"Kardum Cvitan",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/205697/images/5186_n.jpg",email:"kristina.k@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. Whether that be identifying an exceptional author and proposing an editorship collaboration, or contacting researchers who would like the opportunity to work with IntechOpen, I establish and help manage author and editor acquisition and contact."}},relatedBooks:[{type:"book",id:"7476",title:"Land Use",subtitle:"Assessing the Past, Envisioning the Future",isOpenForSubmission:!1,hash:"5b0c406adac8447ffeb089e29eac8ea9",slug:"land-use-assessing-the-past-envisioning-the-future",bookSignature:"Luís Carlos Loures",coverURL:"https://cdn.intechopen.com/books/images_new/7476.jpg",editedByType:"Edited by",editors:[{id:"108118",title:"Dr.",name:"Luis",surname:"Loures",slug:"luis-loures",fullName:"Luis Loures"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"8295",title:"Landscape Reclamation",subtitle:"Rising From What's Left",isOpenForSubmission:!1,hash:"1fb7d9e280708a190a90c3b352c93d45",slug:"landscape-reclamation-rising-from-what-s-left",bookSignature:"Luis Loures",coverURL:"https://cdn.intechopen.com/books/images_new/8295.jpg",editedByType:"Edited by",editors:[{id:"108118",title:"Dr.",name:"Luis",surname:"Loures",slug:"luis-loures",fullName:"Luis Loures"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"5962",title:"Estuary",subtitle:null,isOpenForSubmission:!1,hash:"43058846a64b270e9167d478e966161a",slug:"estuary",bookSignature:"William Froneman",coverURL:"https://cdn.intechopen.com/books/images_new/5962.jpg",editedByType:"Edited by",editors:[{id:"109336",title:"Prof.",name:"William",surname:"Froneman",slug:"william-froneman",fullName:"William Froneman"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophanides",surname:"Theophile",slug:"theophanides-theophile",fullName:"Theophanides Theophile"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"41232",title:"Hydrosurgery-System® in Burn Surgery – Indications and Applications",doi:"10.5772/51851",slug:"hydrosurgery-system-in-burn-surgery-indications-and-applications",body:'Apart from the extent and depth of burns, inflammatory reactions and infections (caused by impurities, cell detritus, bacterial degradation etc.) impair the healing of burn wounds. Bacterial colonization and invasion significantly influence wound healing (epithelialisation and contraction of the wound) [1]. Early debridement and depth-specific early coverage are currently the standard in the surgical treatment of burns [2,3,8,10]. Basic prerequisites are exact determination of the depth and accurate debridement. Particularly in cases of large burn wounds it is essential to preserve and protect vital tissue. In cases of wide, generous removal of tissue by the use of the Dermatom, Guilon or Humbey knife, one frequently removes more than the actual burned tissue and unnecessarily damages vital tissue. On the other hand, one may remove too little necrotic tissue. The depth of the burn may be difficult to difficult to assess so that the surgeon waits too long, causing valuable time to lapse during which he may well have performed surgical repair. Accurate ablation of the damaged layers of skin and identification of petechial bleeding help to assess the vitality of tissue. This permits exact determination of depth (whether the subpapillary, cutaneous or subdermal plexus are preserved) [9,16] and depth-specific coverage.
Versajet® is a hydrosurgical system employing a jet of water by which tissue is simultaneously cut, ablated, and suctioned. The wound is rinsed without significant aerosolisation. This system has been approved by the US Food and Drug Administration (FDA) for debridement of wounds and soft tissue as well as CE-certified for ablation of tissue and other substances in various surgical procedures including wound debridement [7]. The system is based on the Venturi principle: a thin high-velocity jet of water consisting of sterile saline is discharged from a 0.12-mm nozzle into a suction tube (see Table 1). The consistency of the working tip and the velocity of the water jet create a vacuum below the incision window. This aspirates, cuts and suctions the tissue. As the handpiece is held parallel to the wound the high-pressure water jet acts as a scalpel. When the working tip is tilted slightly the scalpel effect of the water jet is reduced while the rinsing and suction effect is enhanced. Furthermore, the quantity of ablated tissue is determined by the pressure settings at the console (1-10), the pressure exerted by the surgeon, and the speed at which the handpiece is moved on tissue. The console is operated by a foot pedal. Hydrosurgical systems have been in use for a large variety of indications [14]. However, they have not entered burn surgery thus far. Further development of the concept led to a more modern system, namely the Versajet® system, which works precisely and simply. A number of handpieces are currently available for various purposes. They differ in terms of the size of the surgical window and the angle of the working tip: 8 mm surgical window, 45° angle, 14 mm surgical window, 15° or 45° angle of the working tip. Furthermore, the different holders are also available in a Versajet plus® variation which enables the surgeon to forcefully ablate tough tissue.The basic principles underlying this concept were derived from histological investigations. The exact layer-wise removal of tissue components achieved by this procedure is of the same quality as that achieved by laser ablation. The Versajet system® was also successfully used for the treatment and the removal of dirt-tattoos/pigment deposits.
\n\t\t\t\t | \n\t\t\t\n\t\t\t\t | \n\t\t\t\n\t\t\t\t | \n\t\t
1 | \n\t\t\t90 ml/min | \n\t\t\t103 bar 426 km/h | \n\t\t
3 | \n\t\t\t125 ml/min | \n\t\t\t265 bar 591 km/h | \n\t\t
7 | \n\t\t\t188 ml/min | \n\t\t\t587 bar 885 km/h | \n\t\t
10 | \n\t\t\t230 ml/min | \n\t\t\t827 bar 1078 km/h | \n\t\t
Physical data
Figures 1 to 5 show a 6-year old boy with partial to full thickness scalds in the neck. Large portions of the chest were also affected. Necrosectomy with Versajet® (at levels 5–7) and subsequent coverage with unmeshed split-thickness skin graft were performed on the 4th day after the accident. Fat gauze was placed on the grafts. A collar was provided to protect the grafts and immobilize the neck postoperatively. On the 6th postoperative day the split-thickness skin grafts had healed in a stable manner. Bacterial investigations performed before and after the treatment showed no microbial growth. The functional outcome after six months was favourable.
6-year-old boy, grade partial to full thickness scalds in the chest and neck, 11% of body surface.
Necrosectomy with Versajet®.
After necrosectomy.
Split-thickness skin graft, unmeshed
10 days postoperatively
Fig. 6 to 10 show a 45-year-old man who developed partial to full thickness-burns in both hands and partial thickness burns in the forearm and face during a car accident. Necrosectomy with Versajet® (at levels 3–5) and split-thickness skin grafting on the dorsum of the left hand were performed on the 2nd day after the accident. The hand covered with a split-thickness skin graft was covered with fat gauze and immobilized with a splint for 6 days. The remaining burned areas were superficially cleaned with Versajet® (at level 3) and treated with Acticoat because the smears showed colonization of germs in the wounds. On the 6th postoperative day the split-thickness skin grafts had healed in a stable manner. The smears showed no microbial growth. Function and aesthetics were satisfactory after six months.
45-year-old man, grade partial thickness burns on both hands
45-year-old man, grade partial thickness burns on both hands
Post debridement
6 months postoperatively, the left hand is covered with a split-skin graft while the right hand was treated by conservative means
6 months postoperatively, the left hand is covered with a split-skin graft while the right hand was treated by conservative means
Fig. 11 to 12 show a 40-year-old man who partial thickness burns in the face covered with pigment deposits after an explosion. Dirt tattoos has been removed by using the hydro surgery system at level 3 with a very superficial removal of the pigment deposits. Uneventful healing shows a clean skin after 2 weeks without scarring.
The experience shows that in cases of full thickness burns a necrosectomy with the Dermatom, Humbey knife or the scalpel could be performed rapidly and efficiently. In these cases Versajet® was of use only in marginal zones or to provide the wound with the necessary finishing touches. Tissue damaged in a leathered fashion could not be ablated rapidly or satisfactorily even by the use of Versajet plus®. In contrast, the advantages of Versajet in the treatment of partial thickness burn wounds are worthy of mention. In particular, burns in complex, inaccessible areas are an indication for the use of this hydrosurgical system. In the region of the face (the lips, eyelids, etc.) debridements can be performed with a degree of precision that is hardly achievable by the use of conventional methods. Furthermore, necrosectomy in the region of the hand (fingers, interdigital spaces, etc.) can be significantly improved by the use of Versajet®. In burn surgery convex surfaces could be ablated uniformly and concavities curetted with precision. Pigment deposits could be completely removed. Histological investigations prove and confirm the precision of ablation by the use of Versajet®.
Fig. 13: This technique permits ablation of clearly defined anatomical structures. Removal of the most superficial layers of skin, dermal papillae/papillary dermis (Fig. 13a). Layer of the superficial reticular dermis, removal of the epidermis, the papillary dermis, and superficial portions of the reticular dermis (Fig. 13b). Layer of the mid reticular dermis (Fig. 13c).
a to c, Layer-wise ablation with Versajet®, a. papillary layer, b reticular layer in the middle, c Reticular layer, deep
In cases of large partial thickness burns this method was very helpful to achieve effective wound debridement. At level 2-3, impurities, coatings and cell detritus could be removed in a simple, rapid and gentle manner and microbial growth could thus be reduced. Smears and biopsies taken before and after the treatment showed marked reduction of microbial growth in all cases. In superficial wounds that could be treated with Versajet® we observed more rapid re-epithelialisation compared to conservative treatment on the side with the same depth of burns treated with fat gauze. In no case did we encounter side effects or undesired events. Steps, unevenness or ridges in tissue were caused by lack of practice, but could be corrected during the procedure. Postoperative wound dressing was performed according to the general guidelines of burn treatment.
Using
As rapid debridement and immediate deep coverage should be performed for the reasons mentioned at the beginning of this report as well as to avoid the risk of hypertrophic scar formation [12], Versajet® fulfils standards of precision, rapid intervention and simple handling. The special domain of Versajet® is partial thickness burns, particularly in poorly accessible anatomical regions [4,13]. These regions can be treated and debrided more effectively by the use of hydrosurgical systems than with conventional methods. By means of layer-wise ablation the surgeon is able to identify healthy tissue immediately and protect it in the best possible manner. Intraoperative diagnosis of the depth of burns is also achieved by this procedure. Owing to these advantages the Versajet® system has become a standard procedure in burn surgery.
Non-alcoholic fatty liver disease (NAFLD) is currently the most prevalent chronic liver disease worldwide [1]. A subset of NAFLD patients have the progressive form of NAFLD termed non-alcoholic steatohepatitis (NASH). NASH is typically characterized by a specific pattern on liver histology, including steatosis, lobular inflammation, and ballooning with or without perisinusoidal fibrosis [2]. It can progress to advanced fibrosis, cirrhosis, hepatocellular carcinoma, and liver-related morbidity and mortality. Liver disease is only the third leading cause of death in patients with NAFLD, following cardiovascular disease and malignancy [3].
\nPrecise histological diagnosis of NAFLD is commonly based on liver biopsy [4]; however, biopsies present several potential problems [5]. Thus, there is a need for reliable and cost-effective noninvasive biomarkers to avoid the invasiveness of biopsy [6].
\nAlthough there are some clinical strategies to ameliorate NAFLD progression, such as treatments for obesity or type 2 diabetes mellitus (T2DM), there is no medication proven to be effective as a treatment for NASH [7]. Therefore, it is necessary to improve the research on possible therapeutic targets for NASH due to the severity of this pathological condition.
\nPrevious evidences have linked gut dysbiosis with obesity, insulin resistance (IR), metabolic syndrome (MS), and NAFLD [8, 9]. The impact of the GM on NAFLD/NASH has been attributed to increased gut permeability, intestinal endotoxemia, endogenous alcohol production, upregulation of hepatic de novo lipogenesis and triglyceride synthesis, reduction in choline metabolism, and aggravation of IR [10]. The increased permeability of the intestinal barrier results in the release of substances such as lipopolysaccharides (LPS), bacterial components, short-chain fatty acids (SCFAs), bile acids (BAs), choline metabolites, and endogenous ethanol that reach the liver and seem to contribute to the pathogenesis of NAFLD (Figure 1) [11, 12]. It is important to note that some of these substances could perhaps be employed as potential noninvasive biomarkers of NAFLD progression.
\nImplication of intestinal dysbiosis in NAFLD pathogenesis. Short-chain fatty acids (SCFAs), bile acids (BAs), lipopolysaccharides (LPS), trimethylamine-N-oxide (TMAO), ethanol (EtOH), non-alcoholic fatty liver (NAFL), and non-alcoholic fatty liver disease (NAFLD).
Manipulation of the microbiota through probiotics, prebiotics, and antibiotic treatment yields encouraging results for the treatment of obesity, T2DM, and NASH in animal models, but data in humans are scarce. In regard to NAFLD, this therapeutic strategy seeks to prevent the endotoxicity produced by the microbiota-derived metabolites that reach the liver and promote the progression of the disease [13]. Thus, there is a need to focus research on the GM as a therapeutic target to ameliorate NASH.
\nTo provide a broad overview of the relationship between intestinal dysbiosis and NAFLD, we have elaborated on this subject in this book chapter. In this sense, this narrative chapter will explain (a) non-alcoholic fatty liver disease, (b) the gut microbiota, (c) gut microbiota-derived mediators involved in NAFLD, and (d) the gut microbiota as a therapeutic target in NAFLD.
\nNAFLD has emerged as the most common form of chronic liver disease worldwide. The incidence of NAFLD has drastically increased in parallel with obesity in recent years. Currently, the global prevalence of NAFLD is approximately 25% [1], but it can increase to 58% in individuals who are overweight or as high as 98% in individuals with nondiabetic morbid obesity [14].
\nNAFLD comprises a spectrum of disorders extending from simple steatosis (SS) to NASH, fibrosis, and cirrhosis [2, 15]. This pathology has potentially serious sequelae [16]. Although SS tends to develop into a favorable clinical course [3], NASH can develop into liver cirrhosis and hepatocellular carcinoma [15]. Thus, liver-related mortality increases exponentially with an advance in the fibrosis stage [17]. In this regard, NASH is a very common cause of liver transplant worldwide [1]. Although the most common cause of death in patients with NAFLD is cardiovascular disease, independent of other metabolic comorbidities, NAFLD is becoming a major cause of liver disease-related morbidity (e.g., cirrhosis, end-stage liver disease, hepatocellular carcinoma, and liver transplantation).
\nNAFLD is characterized by significant lipid deposition in the hepatocytes of the liver parenchyma [18]. Obesity, T2DM, dyslipidemia, MS, and IR are the main risk factors for NAFLD [19]. Most NAFLD patients are asymptomatic, and the evidence of hepatic steatosis should be detected via a routine blood test, showing a deregulation in liver enzymes. Currently, it is not possible to diagnose NAFLD with only a blood test, but the aspartate aminotransferase (AST)-alanine aminotransferase ratio (ALT) can be used as a first step [20, 21, 22]. However, the ALT level correlation with histological findings has poor sensitivity and specificity for the diagnosis of NASH [23]. Then, it is necessary to rule out other causes of liver damage, such as alcoholic fatty liver disease, drug-induced liver injury, viral hepatitis, autoimmune liver disease, hemochromatosis, celiac disease, and Wilson’s disease [1]. Finally, ultrasonography is the most common noninvasive tool used to detect NAFLD. There are also other imaging techniques used to detect liver steatosis, such as computer tomography or magnetic resonance imaging, but ultrasound is the technique that provides the most information without irradiation [24, 25].
\nOne-third of the NAFLD-affected subjects progress to NASH. This condition is characterized by the presence of hepatocellular ballooning and inflammation and has a prevalence of 2–3% worldwide [2]. Key issues in NAFLD patients are the differentiation of NASH from SS and the identification of advanced hepatic fibrosis. To date, liver biopsy has been the
Regarding NAFLD therapeutics, all forms of treatment of metabolic disorders are able to modify liver damage. Diet and lifestyle modification and insulin-sensitizing agents appear to be promisingly effective against NAFLD progression. However, these approaches may not be effective in some patients. Many other drugs are currently being studied to establish treatments for NAFLD. At present, no accepted drug treatment for NASH has been stated [24]. In this sense, it is very important to improve the knowledge of NAFLD physiopathology. Actually, the underlying precise mechanisms of NAFLD pathogenesis have just begun to be understood. The classic “multiple hit” theory states that lipid accumulation initiates hepatic steatosis and subsequently triggers multiple insults acting together (hormones/adipokines from adipose tissue, inflammation, deregulated fat metabolism, lipotoxicity, oxidative stress, mitochondrial dysfunction, and genetic and epigenetic factors), ultimately inducing NASH and cirrhosis [27]. Progression to NASH is linked to systemic inflammation, and it is associated with other pathological processes, such as innate immunity alterations, endoplasmic-reticulum stress, toll-like receptor (TLR) signaling, mitochondrial dysfunction, and intestinal dysbiosis [6, 28, 29, 30, 31, 32]. Regarding this last process, approximately 70–75% of blood that reaches the liver comes from the portal vein circulation that communicates the liver with the intestine [33]. The liver is continually exposed to GM-derived mediators, including bacteria and bacterial components, such as LPS, promoting an inflammatory response that contributes to liver injury [13].
\nMillions of symbiotic microorganisms live on and within human beings and play an important role in human health and disease. Initial colonization occurs at the time of birth, and humans progressively acquire ∼1014 bacterial cells at equilibrium, which remain for life [13].
\nThe human microbiota, especially the GM, has even been considered to be an “essential organ,” carrying approximately 150 times more genes than the human genome [34]. The GM is composed of an immense number of microorganisms (bacteria, viruses, and fungi) with several functions, such as host nutrition, bone mineralization, immune system regulation, xenobiotic metabolism, proliferation of intestinal cells, and protection against pathogens [35, 36]. This bacterial community is dominated by anaerobic bacteria and includes 500–1000 species [37].
The duodenum and proximal jejunum normally contain small numbers of bacteria, usually lactobacilli and enterococci, which are facultative anaerobes. The distal ileum is a transition zone between sparse populations of aerobic bacteria of the proximal small intestine and very dense populations of anaerobic microorganisms in the large bowel. Occasional groups of bacteria can be found in low concentrations within the lumen of the small intestine. Bacteria do not form clusters, and the luminal contents are separated from the mucosa by a mucus layer [13].
\nThe GM is specific to an individual and highly resilient to changes. However, it can be affected by several factors, intrinsic and extrinsic to the host, such as the subject’s genetic makeup, dietary habits, antibiotic use, and environmental changes [13, 39, 40]. A disruption in the composition of the normal GM is known as intestinal dysbiosis [41, 42]. Generally, this process includes an unfavorable change in the bacterial composition, with a reduction in autochthonous bacteria and growth of others that prejudice host health [43].
\nIntestinal dysbiosis is a process that may adversely impact metabolism and produce immune responses, favoring NAFLD progression. Important studies on the relationship of the GM with obesity have identified profound changes in the composition and metabolic function of the GM in subjects with obesity. Moreover, these studies demonstrated that the GM interacts with host epithelial cells to indirectly control energy expenditure and storage and activate inflammatory responses in NASH pathogenesis [44]. Qualitative or quantitative imbalances in the GM might have serious health consequences for the host, including small intestinal bacterial overgrowth (SIBO) syndrome [13]. Due to gut dysbiosis, there is an elevated production of toxic bacterial components and metabolic mediators, which consequently accumulate in the intestine. In addition, an increase in intestinal permeability and further disruption of the epithelial barrier lead to the release of these GM-derived mediators [42], which could reach the liver through portal circulation, favoring hepatic inflammation and the development of NAFLD [45, 46]. After disruption of the gut epithelial barrier, the liver is exposed to microbial products and metabolites resulting from bacterial metabolism [47, 48]. In this sense, it has been demonstrated that patients with NAFLD have gut dysbiosis, gut epithelial barrier dysfunction, and increased translocation of bacterial components to the liver [49]. For this reason, mediators derived from gut dysbiosis might also be related to the pathogenesis of the disease. Several previous studies in clinical settings have associated intestinal dysbiosis with the occurrence of NAFLD [50, 51, 52] and with the progression to NASH [10, 53].
\nAmong the various factors, dietary habits are considered to be most influential on the gut microbiome in subjects with obesity and NAFLD patients. It is well-known that a high-fat diet causes gut dysbiosis characterized by lowered species richness and changes in microbial composition, such as decreased
GM-derived mediators resulting from intestinal dysbiosis could play a key role in NAFLD progression through several mechanisms: (1) enhanced energy extraction from food nutrients by formation of SCFAs; (2) modulation of BA synthesis, which is crucial for fat absorption and affects metabolism of glucose via farnesoid X receptor (FXR); (3) innate immune system activation by bacterial component translocation; (4) endogenous ethanol production; and (5) reduction in choline metabolism, which reduces efflux of very-low-density lipoprotein (VLDL) from hepatocytes, promoting inflammation. These mechanisms involve translocation of these mediators, such as SCFAs, BAs, endogenous ethanol, and choline metabolites, which may be potentially evaluated as noninvasive blood markers of NAFLD progression [59].
\nSCFAs are molecules with seven carbon atoms or less, for example, acetic, propionic, and butyric acids, that are produced by the gut bacterial fermentation of cellulose, xylans, resistant starch, or inulin since humans lack enzymes that digest fibers. These substances can strongly regulate host metabolism [60]. In general, these SCFAs have several effects on energy metabolism, the immune response, and adipose tissue expansion and act as signaling molecules between the GM and the host. SCFAs provide not only important sources of nutrients and energy for the intestinal epithelium but also serve as precursors for lipogenesis and gluconeogenesis [61, 62]. SCFAs can directly act as lipid precursors in the liver and mediate other effects as ligands for G protein-coupled receptors, specifically the subtypes GPR41 and GPR43 [59]. Experimental studies have demonstrated that these SCFAs can modulate regulatory T-cell expansion and enhance neutrophil chemotaxis, promoting inflammation in mouse models [63, 64, 65, 66]. Furthermore, SCFAs modulate the production of several inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin 2 (IL-2), interleukin 6 (IL-6), and interleukin 10 (IL-10) [67]. Recently, some studies found that high concentrations of intestinal SCFAs as a result of dysbiosis and their G-protein coupled receptors play an important role in NAFLD progression [68, 69]. Activation of GPR41 and GPR43 stimulates secretion of peptide-YY, inhibits gut motility, and slows intestinal transit. Therefore, nutrient absorption and energy capture from the diet increase and may promote hepatic lipogenesis [56, 70]. Additionally, activation of GPR41 and GPR43 induces secretion of glucagon-like peptide-1 (GLP-1), which activates genes in hepatocytes that regulate fatty acid β-oxidation and insulin sensitivity [56, 71], promoting NAFLD occurrence and progression. Furthermore, clinical studies have demonstrated SCFA enrichment in fecal samples of children and adults with NAFLD [72, 73].
\nHowever, other previously published studies have reported that SCFAs could be beneficial in the progression of NAFLD. In this regard, butyrate activates AMP-activated protein kinase (AMPK) in the liver and accelerates the assembly of tight junction proteins [74, 75], improving intestinal barrier dysfunction and reducing metabolic endotoxemia. In addition, butyrate is able to modulate regulatory T-cell activity, suppressing the immune response and reducing liver inflammation [76].
\nThe close relationship between intestinal dysbiosis and SCFA production, according to the results of previous experimental and clinical studies, provides evidence of their potential use as markers of NAFLD progression. In this sense, in a recent study, we studied this possibility, but we failed to demonstrate any relationship between circulating SCFA levels and histological degrees of NAFLD in a cohort of patients with morbid obesity [6]. However, additional studies are necessary to accurately determine the specific role of SCFAs in NAFLD.
\nAs previously mentioned, the gut-liver axis, which involves gut hormone release and the immune response, is essential to regulate systemic metabolism. BAs participate in communication along this axis. They are steroid-derivative components of bile synthesized after cholesterol oxidation by enzymes present in hepatocytes, and they are involved in the absorption of lipids and vitamins in bile salt-dependent flow regulation. BAs participate in the digestion and solubilization of lipids and regulate hepatic glucose and inflammation [59, 60]. Moreover, they are capable of controlling their own synthesis through the activation of FXR [77, 78]. In addition, BAs act as signaling molecules that modulate several physiological processes, and GM dysbiosis can change BA pool characteristics through its effects on BA metabolism [78, 79].
\nThe GM is a critical modulator of BA pool size and composition, and the process of dysbiosis could substantially alter concentrations of conjugated and/or secondary bile acids, as well as increase their synthesis.
\nUnmodified BAs, also called primary BAs (cholic acid (CA) and chenodeoxycholic acid (CDCA)), undergo a deconjugation process by GM components after reaching the colon and become secondary BAs, such as deoxycholic acid (DCA) and lithocholic acid (LCA); they can be transported again to the liver via the portal vein in a mechanism called “enterohepatic circulation.” BAs prevent the overgrowth of bacteria in the gut to maintain gut homeostasis. This protective effect is mediated by their detergent properties and the activation of FXR, which protects the distal small intestine from bacterial proliferation. It is recognized that these circulating BAs, in addition to the abovementioned functions, can coordinate a wide number of pathways mediated by specific nuclear receptors (NRs) [60].
\nThe increased intestinal permeability associated with BA modifications has been linked to metabolic endotoxemia, IR, and inflammatory cytokine release with enhanced proinflammatory signaling cascades, which are common findings in patients with NAFLD [59]. An increased level of BAs causes activation of the cell death pathway mediated by inflammatory and oxidative stress cascades in liver tissue [80, 81].
\nRegarding hepatic lipid metabolism, Watanabe et al. demonstrated that hepatic FXR activation mediated by BAs could induce the expression of the atypical NR small heterodimer partner (SHP), which promotes the inhibition of sterol-regulatory element-binding protein-1c (SREBP-1c), thus reducing hepatic synthesis of triglycerides. In addition, FXR can limit lipid accumulation in the liver by promoting fatty acid oxidation after the activation of peroxisome proliferator-activated receptor alpha (PPARα) and by the induction of plasma VLDL-triglyceride clearance [82, 83, 84, 85]. FXR activation in the liver was also demonstrated to coordinate glucose homeostasis via the inhibition of gluconeogenesis and glycolysis. Interestingly, the activation of FXR in the intestine can generate crucial endocrine feedback regulation [86]. Experimental studies have demonstrated that intestinal dysbiosis can modulate the activity of FXR in the intestine, affecting lipid metabolism in the liver [4]. Specifically, FXR not only plays an important role in maintaining BA levels but also regulates glucose and lipid metabolism via different mechanisms, such as increasing insulin sensitivity, repressing hepatic gluconeogenic genes, and increasing hepatic glycogen synthesis [87, 88].
\nPrevious investigations have demonstrated a BA level increase in the biological fluids of patients with NASH compared to that in the biological fluids of subjects with healthy livers and an evident association with intestinal dysbiosis [89, 90, 91]. Additionally, the levels of BAs have been correlated with histopathological features, such as the degree of hepatic steatosis, the presence of cellular ballooning, and the severity of fibrosis in patients with NASH [92]. These studies confirmed the disruption in BA homeostasis in NASH physiopathology [65] and the correlation of BAs with NASH severity parameters (portal inflammation, lobular inflammation, and hepatocyte ballooning) [93]. In children with NAFLD, changes in the circulating BA profile have also been reported. Troisi et al. demonstrated that serum BA levels decrease in early NAFLD and increase during progression to fibrosis in obese children. These authors postulated that BAs may have value as a noninvasive biomarker in pediatric NAFLD progression [83, 94]. In a previous study by our research group, we found that FXR jejunal expression was lower in NASH patients than in normal liver (NL) subjects; in regard to BAs, we also found that levels of glycolic acid (GCA), a primary BA, and DCA, a secondary BA, were significantly higher in NAFLD patients than in NL subjects [6].
\nConsidering the numerous published experimental and clinical studies associating gut dysbiosis, BAs and NAFLD, it is expected that BAs could be proposed as potential noninvasive markers of the disease. For example, Svegliati-Baroni et al. specifically proposed DCA and LCA, which can only be produced by bacterial fermentation [95].
\nThe liver is exposed to potentially harmful substances derived from the gut, considered pathogen-associated molecular patterns (PAMPs), that include translocated bacteria, LPS, bacterial DNA, bacterial RNA, and endotoxins, which are potent inducers of tissue inflammation [41, 96]. These PAMPs might contribute to the pathogenesis of NAFLD by activating the innate immune system via TLRs, which recognize these gut-derived bacterial components. The healthy liver expresses low mRNA levels of TLRs (TLR1, TLR2, TLR4, TLR6, TLR7, TLR8, TLR9, and TLR10), implying a high tolerance of the liver to TLR ligands from the microbiota. The translocation of these bacterial components from the gut into the portal system is facilitated by intestinal barrier disruption due to GM dysbiosis [13, 96]. In this sense, there is evidence that dysbiosis causes permeability changes that increase portal levels of gut-derived TLR ligands (LPS or endotoxin), which further activate TLR4 on hepatic Kupffer and stellate cells [97]. LPS is the major structural component of gram-negative bacteria and the major component of endotoxin. LPS may be recognized by LPS-binding protein (LBP) in serum and is the major activator of the innate immune response [98]. Ruiz et al. indicated that the serum levels of LBP were increased in patients with obesity and NASH compared to those in patients with obesity and SS and the increased serum LBP level was correlated to an upregulated expression of TNF-α in liver tissue [99].
\nDuring TLR4 activation, the adaptor molecule myeloid differentiation factor 88 (MyD88) is activated, and the downstream signaling MyD88-dependent pathway results in the activation of necrosis factor kappa beta (NF-κB), leading to the expression of proinflammatory cytokines (TNF-α, IL-6, IL-8 and IL-12) and chemokines (interferon γ (IFN-γ) and monocyte chemotactic protein-1 (MCP-1)), promoting inflammation [68, 97]. There are several intracellular cascades involved in this process, generating oxidative stress, low-grade systemic inflammation, and hepatic injury [100]. In addition, TLR signaling can also lead to the production of inflammasomes in peripheral and parenchymal cells, which activate a variety of processes, including activation of caspase-1, resulting in cell death [101].
\nThe inflammasome, which is a multimeric signaling platform that leads to the production of IL-18 and IL-1β through the NOD-like receptors pyrin domain-containing (NLRP3 and NLRP6), is activated by LPS derived from intestinal dysbiosis via TLR4 and TLR9 responses. Reports have associated inflammasome activation with the development of liver steatosis, inflammation, and fibrosis in NAFLD patients [102, 103].
\nIt has been shown that TLR2, TLR4, and TLR9 play an important role in the development of NASH [104]. In addition, other studies have established that the increase in endotoxin levels is related to IL-1α and TNF-α production [105, 106]. In patients with NAFLD, gut permeability and SIBO due to intestinal dysbiosis have been associated with the severity of steatosis [107]. In biopsy-proven human NASH, plasma levels of IgG against endotoxin were found to be increased with NASH grade severity, suggesting the deleterious effect of chronic endotoxin exposure [108]. In our previous GM-derived metabolite study, we found overexpression of TLR9 jejunal expression in NAFLD subjects, which suggested the activation of the immune system during NAFLD progression [6]. Additionally, enhanced expression of TLR4, the release of IL-8, and high levels of LPS have been demonstrated in NAFLD patients [109, 110]. However, other reports did not reveal an association between endotoxemia and NAFLD progression, suggesting that endotoxemia may not be the only driver of disease development in all patients [111].
\nMultiple experimental studies have demonstrated that a high-fat diet can increase the proportion of LPS derived from the GM, and administration of endotoxin has been shown to induce IR and weight gain [99, 112]. On the other hand, some authors have recently proposed that the small intestine shields the liver from otherwise toxic fructose exposure via the GM [113].
\nThere is a clear relation between gut dysbiosis, bacterial-derived components, the inflammatory response, and NAFLD; therefore, these bacterial mediators, especially circulating TLRs, might be used as potential noninvasive markers of disease progression.
\nIntestinal dysbiosis increases endogenous ethanol production [111], which also affects gut permeability, disrupting intestinal tight junctions. This process allows endotoxins and ethanol to reach the liver and trigger the TLR response and inflammasome activation, contributing to liver damage [114]. In addition to the proinflammatory response, ethanol promotes oxidative stress and hepatocyte necrosis because of the formation of reactive oxygen and nitrogen species [94]. Endogenous ethanol inhibits the tricarboxylic acid cycle, thus increasing levels of acetate and thereby promoting triglyceride accumulation in hepatocytes [64]. Ethanol can also increase the activity of the enzyme cytochrome P450 2E1 (CYP2E1), which catalyzes the oxidation of ethanol but produces free radicals favoring oxidative damage, mitochondrial dysfunction, and liver inflammation [94, 115, 116].
\nSeveral studies have detected increased levels of non-dietary ethanol derived from bacteria in patients with obesity [111, 117] and in patients with NASH [111, 118, 119]. In this sense, Zhu et al. proposed that microbiomes rich in ethanol-producing
Furthermore, Zhu et al. showed an increased abundance of alcohol-producing bacteria in NASH microbiomes, elevated blood-ethanol concentration in NASH patients, and the well-established role of alcohol metabolism in oxidative stress and liver inflammation [56]. In our previous GM-derived metabolite study, we found an interesting result about the higher circulating endogenous ethanol levels in NASH patients than in patients with SS. This fact suggested that circulating ethanol levels could distinguish between different degrees of liver damage. Moreover, in the same study, we evaluated the diagnostic efficacy of a biomarker panel including circulating ethanol, betaine, GCA, and DCA levels as markers of NASH in a group of patients with liver histology indicative of NASH. A cutoff point and area under the curve were determined so that NASH could be diagnosed. The accuracy with which this panel discriminates NASH subjects from non-NASH subjects showed an area under the ROC curve (AUROC) of approximately 0.776 (0.632–0.921). Therefore, we concluded that the levels of certain circulating microbiota-related metabolites are associated with NAFLD severity and could be used as a “liquid biopsy” in the noninvasive diagnosis of NASH [6].
\nIn summary, proinflammatory and prooxidative damage has been demonstrated as a result of endogenous ethanol in the liver, which might contribute to the pathogenesis of NAFLD, and previous reports may support its use as a noninvasive biomarker of disease progression.
\nCholine is an essential nutrient obtained through both dietary intake and endogenous synthesis and is an important constituent of the phospholipid membrane. The human GM actively metabolizes dietary components, including choline. Alterations in choline and phosphatidylcholine metabolism due to intestinal dysbiosis may have an impact on several physiological pathways, which could induce NAFLD. Choline deficiency prevents the synthesis and excretion of VLDL, leading to hepatic triglyceride accumulation and liver steatosis [122, 123]. In fact, the link between choline deficiency and the accumulation of hepatic lipids has been recognized for more than 50 years [124], leading to the establishment of choline-deficient diets to induce models of NAFLD in animals.
\nIn addition, choline can be metabolized to its derivative trimethylamine (TMA) by the GM. TMA reaches the liver via portal circulation and is subsequently oxidized by hepatic flavin-containing monooxygenases in the liver, forming trimethylamine-N-oxide (TMAO), which is then released into blood circulation [125, 126]. Previous studies have revealed that TMAO may affect lipid absorption and cholesterol homeostasis and modulate glucose and lipid metabolism by decreasing the total BA pool size [122]. TMAO modulates glucose metabolism and increases IR in mice fed a high-fat diet [127]. TMAO also affects lipid absorption and cholesterol homeostasis by reducing the conversion of cholesterol into BAs [122].
\nA small number of human studies have shown that the consumption of a low-choline diet promotes fatty liver and liver damage [123, 128]. Other studies have pointed out that plasma-free choline levels are positively related to the severity of NAFLD, fibrosis, and NASH [129, 130].
\nOn the other hand, in our previous research, we analyzed circulating levels of these choline metabolites according to hepatic histology and observed that levels of TMAO were significantly higher in NAFLD patients than in NL subjects [6], which correlates with the previous statement that serum TMAO levels are significantly higher in patients with NAFLD than in healthy people and correlates with the development and severity of NAFLD through different mechanisms: modulating glucose metabolism, promoting inflammation in adipose tissue, and influencing lipid absorption and cholesterol homeostasis [125, 129, 131].
\nIn summary, the evidence has demonstrated that choline and TMAO are associated with the progression of NAFLD, indicating the potential use of these GM-derived mediators as markers of disease progression.
\nAlthough there are no treatments to directly reverse steatosis, fibrosis, or liver damage, lifestyle changes and therapeutic strategies to treat other MS-related diseases, such as obesity, T2DM, or IR, could ameliorate NAFLD, avoiding its progression to NASH. Lifestyle intervention (diet and exercise), bariatric surgery, antidiabetic drugs, lipid-altering agents, and antihypertensive drugs can improve all of the features of NASH by ameliorating MS-related diseases [4]. Nevertheless, there is currently no specific treatment proven to be effective in treating NASH. Clarifying NAFLD risk factors could lead to more accurate prediction of disease progression and more effective treatments based on individualized drivers of disease [132]. The search for a possible therapy for NASH is focused on different pathways: metabolic targets, cell stress and apoptosis, immune targets, fibrosis, and GM modulation.
\nCurrently, there are different mechanisms to manage NAFLD/NASH with metabolic targets focused on ameliorating other related diseases but also involved in NAFLD progression. Moreover, vitamin E acts as an antioxidant and hepatoprotective agent used to treat NASH (Figure 2).
\nCurrent and future treatment strategies to manage and treat NAFLD and NASH. Peroxisome proliferator-activated receptor (PPAR), farnesoid X receptor (FXR), farnesoid growth factor-19 (FGF-19), farnesoid growth factor-21 (FGF-21), acetyl-CoA carboxylase (ACC), glucagon-like peptide-1 receptor (GLP-1R), dipeptidyl peptidase-4 (DPP-4), sodium-glucose cotransporter 1/2 (SGLT-1/2), apoptosis signal-regulating kinase-1 (ASK-1), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and lysyl oxidase-like 2 (LXL-2).
On the other hand, there are many active studies and clinical trials focused on new therapeutic strategies with different pharmacological targets to avoid NAFLD and NASH progression. In this regard, PPAR agonists, antidiabetic drugs, FXR ligands, and anti-inflammatory and antiapoptotic agents can act as insulin sensitizers and improve the proinflammatory chronic state characteristic of NASH; antifibrotic agents can avoid NASH progression to fibrosis; and GM modulation can prevent the intestinal dysbiosis involved in NAFLD pathogenesis (Figure 2) [4, 7, 24, 133].
\nThe key role that the GM plays in the progression of the disease opens the door to new ways of thinking about NASH prevention and treatment. The possibility of modulating the GM to treat NAFLD and NASH has gained interest in the potential use of probiotics, prebiotics, and antibiotics as effective treatments.
\nProbiotics are defined as viable microorganisms that when administered in adequate amounts, confer a health benefit to the host [134]. There are many mechanisms by which probiotics improve the GM and consequently ensure liver health (inhibition of intestinal bacterial enzymes, stimulation of host immunity, competition for limited nutrients, inhibition of bacterial mucosal adherence and epithelial invasion, protection against intestinal permeability, and control of bacterial translocation from the gut to the portal vein circulation). The biological activity of probiotics depends on delivering anti-inflammatory mediators that downregulate proinflammatory cytokines [104]. Therefore, probiotic therapy offers an interesting approach to control hepatic injury and a low-grade proinflammatory state.
\nAnother alternative is the use of prebiotic fiber, which is defined as an amount of nondigestible food ingredients that beneficially affect the host, by selectively stimulating the growth and/or activity of one or a limited number of bacteria in the colon [135]. The health effects of prebiotic fiber are related to improved glucoregulation and modified lipid metabolism as well as selective modulation of the GM. Some mechanisms have been proposed to explain the beneficial effects of prebiotics on the accumulation of triglycerides in the liver observed in animals, including reduced de novo fatty acid synthesis and SCFA production, body weight and fat loss, and improved glycemic control, GM modulation, and anti-inflammatory effects [13, 104]. These promising preliminary results strongly indicate the potential use of probiotics and prebiotics for the prevention or treatment of NASH.
\nProphylactic use of antibiotics in patients with chronic liver diseases is an established method of preventing infections or innate immune dysfunction in acute liver failure (ALF) [13]. In addition, it has been demonstrated in animal and human models that the positive effect of polymyxin B and metronidazole in reducing the severity of NAFLD during total parenteral nutrition or after intestinal bypass could be interesting for their use to treat NAFLD [136, 137]. However, direct evidence is currently lacking, and thus, antibiotics cannot be routinely recommended to treat NASH, although further research is needed.
\nOverall, to date, there have been only a few studies concerning the use of probiotics, prebiotics, and antibiotics in humans; therefore, large-scale randomized controlled trials with histological endpoints are indicated.
\nIntestinal dysbiosis can trigger gut inflammation and increase the permeability of the intestinal epithelial barrier, exposing the gut-liver axis to GM-derived mediators of dysbiosis, such as bacterial components or metabolites, which may induce hepatotoxicity, inflammation, and consequently NAFLD progression. Gut-derived mediators of dysbiosis contribute to NAFLD progression by activating the immune system, inducing oxidative stress, enhancing inflammation, and finally promoting fibrogenesis.
\nDespite the evident association between GM dysbiosis, obesity, and NAFLD derived from several experimental studies, few studies have been conducted in patients with NAFLD to explore the role of GM-derived mediators of dysbiosis in the occurrence and progression of the disease. Additionally, few studies have focused on gut-derived mediators of dysbiosis as noninvasive markers of disease progression. The study of these mediators may provide an opportunity to develop a specific diagnostic and prognostic biomarker for NAFLD and NASH. In this sense, we propose the metabolomic study of these mediators and other metabolites involved to achieve a metabolomic profile that could be used as biomarkers for evaluating the status of NAFLD. On the other hand, some previous evidence has focused on GM modulation using probiotics, prebiotics, and antibiotics as therapeutic strategies to prevent or treat NAFLD and NASH, which is more uncertain and requires future research. In this sense, it remains important to promote study of GM targeting to find an effective treatment for NAFLD and overall for NASH.
\nThis study was supported by the
The authors declare no conflict of interest.
NAFLD | non-alcoholic fatty liver disease |
NASH | non-alcoholic steatohepatitis |
GM | gut microbiota |
T2DM | type 2 diabetes mellitus |
IR | insulin resistance |
MS | metabolic syndrome |
LPS | lipopolysaccharides |
SCFAs | short-chain fatty acids |
BAs | bile acids |
TMAO | trimethylamine-N-oxide |
EtOH | ethanol |
NAFL | non-alcoholic fatty liver |
SS | simple steatosis |
AST | aspartate aminotransferase |
ALT | alanine aminotransferase |
TLRs | toll-like receptors |
SIBO | small intestinal bacterial overgrowth syndrome |
FXR | farnesoid X receptor |
VLDL | very-low density lipoprotein |
GPR | G-protein coupled receptors |
TNF-α | tumor necrosis factor alpha |
IL | interleukin |
GLP-1 | glucagon-like peptide-1 |
AMPK | AMP-activated protein kinase |
CA | cholic acid |
CDCA | chenodeoxycholic acid |
DCA | deoxycholic acid |
LCA | lithocholic acid |
NRs | nuclear receptors |
SHP | small heterodimer partner |
SREBP-1c | sterol-regulatory element-binding protein-1c |
PPARα | proliferator-activated receptor alpha |
NL | normal liver |
GCA | glycolic acid |
PAMPs | pathogen-associated molecular patterns |
LPB | LPS-binding protein |
NF-κB | necrosis factor-kappa beta |
INF-γ | interferon gamma |
MCP-1 | monocyte chemotactic protein-1 |
NLRP | NOD-like receptors pyrin domain |
CYP2E1 | enzyme cytochrome P450 2E1 |
AUROC | area under the ROC curve |
TMA | trimethylamine |
FGF | farnesoid growth factor |
ACC | acetyl-CoA carboxylase |
DPP-4 | dipeptidyl peptidase-4 |
SGLT-1/2 | sodium-glucose cotransporter-1/2 |
ASK-1 | apoptosis signal-regulating kinase-1 |
LXL-2 | lysyl oxidase-like-2 |
ALF | acute liver failure |
Supporting women in scientific research and encouraging more women to pursue careers in STEM fields has been an issue on the global agenda for many years. But there is still much to be done. And IntechOpen wants to help.
",metaTitle:"IntechOpen Women in Science Program",metaDescription:"Supporting women in scientific research and encouraging more women to pursue careers in STEM fields has been an issue on the global agenda for many years. But there is still much to be done. And IntechOpen wants to help.",metaKeywords:null,canonicalURL:null,contentRaw:'[{"type":"htmlEditorComponent","content":"At IntechOpen, we’re laying the foundations for the future by publishing the best research by women in STEM – Open Access and available to all. Our Women in Science program already includes six books in progress by award-winning women scientists on topics ranging from physics to robotics, medicine to environmental science. Our editors come from all over the globe and include L’Oreal–UNESCO For Women in Science award-winners and National Science Foundation and European Commission grant recipients.
\\n\\nWe aim to publish 100 books in our Women in Science program over the next three years. We are looking for books written, edited, or co-edited by women. Contributing chapters by men are welcome. As always, the quality of the research we publish is paramount.
\\n\\nAll project proposals go through a two-stage peer review process and are selected based on the following criteria:
\\n\\nPlus, we want this project to have an impact beyond scientific circles. We will publicize the research in the Women in Science program for a wider general audience through:
\\n\\nInterested? If you have an idea for an edited volume or a monograph, we’d love to hear from you! Contact Ana Pantar at book.idea@intechopen.com.
\\n\\n“My scientific path has given me the opportunity to work with colleagues all over Europe, including Germany, France, and Norway. Editing the book Graph Theory: Advanced Algorithms and Applications with IntechOpen emphasized for me the importance of providing valuable, Open Access literature to our scientific colleagues around the world. So I am highly enthusiastic about the Women in Science book collection, which will highlight the outstanding accomplishments of women scientists and encourage others to walk the challenging path to becoming a recognized scientist." Beril Sirmacek, TU Delft, The Netherlands
\\n\\nAdvantages of Publishing with IntechOpen
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\n\nWe aim to publish 100 books in our Women in Science program over the next three years. We are looking for books written, edited, or co-edited by women. Contributing chapters by men are welcome. As always, the quality of the research we publish is paramount.
\n\nAll project proposals go through a two-stage peer review process and are selected based on the following criteria:
\n\nPlus, we want this project to have an impact beyond scientific circles. We will publicize the research in the Women in Science program for a wider general audience through:
\n\nInterested? If you have an idea for an edited volume or a monograph, we’d love to hear from you! Contact Ana Pantar at book.idea@intechopen.com.
\n\n“My scientific path has given me the opportunity to work with colleagues all over Europe, including Germany, France, and Norway. Editing the book Graph Theory: Advanced Algorithms and Applications with IntechOpen emphasized for me the importance of providing valuable, Open Access literature to our scientific colleagues around the world. So I am highly enthusiastic about the Women in Science book collection, which will highlight the outstanding accomplishments of women scientists and encourage others to walk the challenging path to becoming a recognized scientist." Beril Sirmacek, TU Delft, The Netherlands
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His main focus now is to unravel the mechanism of drought and heat stress response in plants to tackle climate change related threats in agriculture.",institutionString:null,institution:{name:"Indian Council of Agricultural Research",country:{name:"India"}}},{id:"4782",title:"Prof.",name:"Bishnu",middleName:"P",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/4782/images/system/4782.jpg",biography:"Bishnu P. Pal is Professor of Physics at Mahindra École\nCentrale Hyderabad India since July 1st 2014 after retirement\nas Professor of Physics from IIT Delhi; Ph.D.’1975 from IIT\nDelhi; Fellow of OSA and SPIE; Senior Member IEEE;\nHonorary Foreign Member Royal Norwegian Society for\nScience and Arts; Member OSA Board of Directors (2009-\n11); Distinguished Lecturer IEEE Photonics Society (2005-\n07).",institutionString:null,institution:{name:"Indian Institute of Technology Delhi",country:{name:"India"}}},{id:"69653",title:"Dr.",name:"Chusak",middleName:null,surname:"Limsakul",slug:"chusak-limsakul",fullName:"Chusak Limsakul",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Prince of Songkla University",country:{name:"Thailand"}}},{id:"75563",title:"Dr.",name:"Farzana Khan",middleName:null,surname:"Perveen",slug:"farzana-khan-perveen",fullName:"Farzana Khan Perveen",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/75563/images/system/75563.png",biography:"Dr Farzana Khan Perveen (FLS; Gold-Medallist) obtained her BSc (Hons) and MSc (Zoology: Entomology) from the University of Karachi, MAS (Monbush-Scholar; Agriculture: Agronomy) and from the Nagoya University, Japan, and PhD (Research and Course-works from the Nagoya University; Toxicology) degree from the University of Karachi. 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