Abstract
Gut barrier integrity is important to maintain homeostasis between intraluminal contents and the sterile internal environment. Several physical and immunological mechanisms exist to support this balance. An inflammatory response may disrupt this delicate balance in the intestine and lead to intestinal barrier failure.
Ingestion of dietary lipids in high concentrations has been shown to preserve intestinal barrier integrity. Several physiological responses are elicited upon ingestion of a high-fat diet that may account for these beneficial effects. Chylomicrons are formed that can neutralize endotoxin via apolipoproteins. Furthermore, ingestion of long chain polyunsaturated fatty acids decreases production of inflammatory mediators and the expression of adhesion molecules. Next to these direct effects, dietary lipids also trigger a newly discovered neuro-immunological pathway via release of cholecystokinin (CCK). Release of CCK triggers the autonomic nervous system leading to a reduction of the inflammatory response and preservation of intestinal barrier integrity via binding of acetylcholine to specific nicotinic receptors. The inflammatory response and intestinal barrier dysfunction play an important role in a number of intestinal disorders such as inflammatory bowel disease and postoperative ileus. Manipulation of the inflammatory response and intestinal barrier integrity via administration of lipid enriched nutrition may provide a new therapeutic opportunity to reduce clinical relevant disorders such as postoperative ileus. In this review we discuss the interaction between lipid enriched nutrition, the autonomic nervous system, inflammation and the intestinal epithelial barrier.Keywords: Inflammation, gut barrier function, high-fat nutrition, vagus nerve, CCK.
Current Nutrition & Food Science
Title:High Fat Diet and Gut Barrier Function
Volume: 9 Issue: 2
Author(s): A.C. van den Heijkant, M.D.P Luyer and W.A. Buurman
Affiliation:
Keywords: Inflammation, gut barrier function, high-fat nutrition, vagus nerve, CCK.
Abstract: Gut barrier integrity is important to maintain homeostasis between intraluminal contents and the sterile internal environment. Several physical and immunological mechanisms exist to support this balance. An inflammatory response may disrupt this delicate balance in the intestine and lead to intestinal barrier failure.
Ingestion of dietary lipids in high concentrations has been shown to preserve intestinal barrier integrity. Several physiological responses are elicited upon ingestion of a high-fat diet that may account for these beneficial effects. Chylomicrons are formed that can neutralize endotoxin via apolipoproteins. Furthermore, ingestion of long chain polyunsaturated fatty acids decreases production of inflammatory mediators and the expression of adhesion molecules. Next to these direct effects, dietary lipids also trigger a newly discovered neuro-immunological pathway via release of cholecystokinin (CCK). Release of CCK triggers the autonomic nervous system leading to a reduction of the inflammatory response and preservation of intestinal barrier integrity via binding of acetylcholine to specific nicotinic receptors. The inflammatory response and intestinal barrier dysfunction play an important role in a number of intestinal disorders such as inflammatory bowel disease and postoperative ileus. Manipulation of the inflammatory response and intestinal barrier integrity via administration of lipid enriched nutrition may provide a new therapeutic opportunity to reduce clinical relevant disorders such as postoperative ileus. In this review we discuss the interaction between lipid enriched nutrition, the autonomic nervous system, inflammation and the intestinal epithelial barrier.Export Options
About this article
Cite this article as:
van den Heijkant A.C., Luyer M.D.P and Buurman W.A., High Fat Diet and Gut Barrier Function, Current Nutrition & Food Science 2013; 9 (2) . https://dx.doi.org/10.2174/1573401311309020005
DOI https://dx.doi.org/10.2174/1573401311309020005 |
Print ISSN 1573-4013 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3881 |
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