Nutrient-induced inflammation in the intestineJi, Yong; Sakata, Yasuhisa; Tso, PatrickCurrent Opinion in Clinical Nutrition and Metabolic Care: July 2011 - Volume 14 - Issue 4 - p 315–321 doi: 10.1097/MCO.0b013e3283476e74 Genes and cell metabolism: Edited by Nada Abumrad Abstract Author InformationAuthors Article MetricsMetrics Purpose of review To review our current understanding of the relationship between absorption of nutrients and intestinal inflammatory response. Recent findings There is increasing evidence linking gut local inflammatory events with the intake of nutrients. Our recent studies, using the conscious lymph fistula rat model, demonstrate that fat absorption activates the intestinal mucosal mast cells. This is accompanied by a dramatic increase in the lymphatic release of mast cell mediators including histamine, rat mucosal mast cell protease II (RMCPII), as well as the lipid mediator prostaglandin D2 (PGD2). Clinical studies suggest that increased consumption of animal fat may play a role in the pathogenesis of inflammatory bowel disease. This impact of dietary fat may not be restricted to the gut but may extend to the whole body. There is evidence linking a high-fat diet-induced metabolic syndrome, with a low-grade chronic inflammatory state. In this review, we hope to convince the readers that fat absorption can have far reaching physiological and pathophysiological consequences. Summary Understanding the relationship between nutrient absorption and intestinal inflammation is important. We need a better understanding of the interaction between enterocytes and the intestinal immune cells in nutrient absorption and the gut inflammatory responses. Department of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, Ohio, USA Correspondence to Patrick Tso, PhD, Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, 2120 E. Galbraith Road, Building A, Cincinnati, OH 45237, USA Tel: +1 513 558 2151; fax: +1 513 558 1006; e-mail: email@example.com © 2011 Lippincott Williams & Wilkins, Inc.