Effects of dietary components on intestinal permeability in health and disease

Abstract

Altered intestinal permeability plays a role in many pathological conditions. Intestinal permeability is a component of the intestinal barrier. This barrier is a dynamic interface between the body and the food and pathogens that enter the gastrointestinal tract. Therefore, dietary components can directly affect this interface, and many metabolites produced by the host enzymes or the gut microbiota can act as signaling molecules or exert direct effects on this barrier. Our aim was to examine the effects of diet components on the intestinal barrier in health and disease states. Herein, we conducted an in-depth PubMed search based on specific key words (diet, permeability, barrier, health, disease, and disorder), as well as cross references from those articles. The normal intestinal barrier consists of multiple components in the lumen, epithelial cell layer and the lamina propria. Diverse methods are available to measure intestinal permeability. We focus predominantly on human in vivo studies, and the literature is reviewed to identify dietary factors that decrease (e.g., emulsifiers, surfactants, and alcohol) or increase (e.g., fiber, short-chain fatty acids, glutamine, and vitamin D) barrier integrity. Effects of these dietary items in disease states, such as metabolic syndrome, liver disease, or colitis are documented as examples of barrier dysfunction in the multifactorial diseases. Effects of diet on intestinal barrier function are associated with precise mechanisms in some instances; further research of those mechanisms has potential to clarify the role of dietary interventions in treating diverse pathologic states.

Keywords: diet; food; gut barrier; microbiota; nutrition.

Graphical abstract

Fig. 1.

Effects of fibers and anthocyanins on the intestinal barrier. Note effects of SCFA on intracellular production of ATP, mucus layer, GLP-2 production, and regulation of immune cells including T cells. ATP, adenosine triphosphate; GLP-2, glucagon-like peptide-2; s-IgA, secretory immunoglobulin-A; SCFA, short-chain fatty acid. One-sided arrow shows activation.

Fig. 2.

Effects of vitamins, zinc, anthocyanins, and polyphenols on the intestinal barrier. Note the effects of vitamins A and D, zinc and anthocyanins on TJ proteins. TJ, tight junction. One-sided arrow shows activation.

Fig. 3.

Effects of fat, proteins and amino acids on the intestinal barrier. Note the effect of amino acids on different intracellular signaling pathways and enzymes, and the effect of gliadin on CXCR3 and TJ proteins. IL-22, interleukin-22, LPS, lipopolysaccharides, TJ, tight junction, ATP, adenosine triphosphate, DNA, deoxyribonucleic acid, CXCR3, chemokine receptor CXCR3; ROS, reactive oxygen species; iNOS, inducible nitric oxide synthase; PXR, pregnane X receptor; AHR, aryl hydrocarbon receptor. One sided arrow shows activation, while dashed arrow shows inhibitory effects.

Fig. 4.

Effects of sugars, ethanol, bile acids, and emulsifiers on the intestinal barrier. Note the effects of glucose on AJ proteins and bacteria, fructose reduces the intracellular ATP, and ethanol alters the bacteria and directly damages the epithelial cells. Note how bile acids affect signaling pathways and emulsifiers exert their effect on TJ proteins. AJ, adherens junction; ATP, adenosine triphosphate; BA, bile acid; FXR, farnesoid X receptor; GLUT5, glucose transporter 5; SGLT1, sodium-glucose linked transporter 1; TGR5, Takeda G protein-coupled receptor 5; TJ, tight junction. One-sided arrow shows activation.