Role of gut barrier function in the pathogenesis of nonalcoholic fatty liver disease

Abstract

Nonalcoholic fatty liver disease (NAFLD) is one of the most common forms of chronic liver disease, and its incidence is increasing year by year. Many efforts have been made to investigate the pathogenesis of this disease. Since 1998 when Marshall proposed the conception of "gut-liver axis, " more and more researchers have paid close attention to the role of gut barrier function in the pathogenesis of NAFLD. The four aspects of gut barrier function, including physical, chemical, biological, and immunological barriers, are interrelated closely and related to NAFLD. In this paper, we present a summary of research findings on the relationship between gut barrier dysfunction and the development of NAFLD, aiming at illustrating the role of gut barrier function in the pathogenesis of this disease.

Rhamnolipids enhance growth performance by improving the immunity, intestinal barrier function, and metabolome composition in broilers

“…The intestinal barrier, which mainly contains physical, chemical, immunological, and microbial barriers, is regarded as the most vital line of defense against pathogens, antigens, toxins, and other harmful substances, preventing them from entering the host 10 . The physical barrier, which consists of the mucous layer, intestinal epithelial cells, and tight membrane junctions, has an extremely important function in regulating intestinal permeability 11 . The chemical barrier consists of gastric acid, various digestive enzymes, glycoprotein mucin, and bacteriostatic substances, which can prevent intestine cell damage and bacterial translocation 12 .…”

Some Approaches to the Therapy of Changes in Intestinal Microbiocenosis in Non-Alcoholic Steatohepatitis

“…В патологический процесс при НАЖБП вовлекаются разные органы и системы, в том числе кишечник [5]. Внимание клиницистов-исследователей в основном уделено роли изменений кишечной микробиоты при НАЖБП [6,7]. В качестве значимого механизма развития и ее прогрессии указывают на нарушения проницаемости кишечного барьера, транслокацию в печень бактерий, вирусов с дальнейшим развитием в ее паренхиме и строме низкоактивного воспаления [8].…”

Intestinally derived bacterial products stimulate development of nonalcoholic steatohepatitis

“…Changes in the function of intestinal tight-junction protein occludin play a major role in increased intestinal permeability. Thus, impairment of tight junctions increases intestinal permeability, which is accompanied by the translocation of microbial products from intestinal lumen to the bloodstream [30,31]. Modulators of this new gut vascular barrier are not yet determined; however, dietary factors, mucosal inflammation of any etiology (such as that involving drugs, infections, or toxins), and hypoperfusion, are currently recognized as disruptors of the intestinal epithelial wall [32].…”

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