Analysis of immunohistomorphological changes in the colonic mucosa in a high-saturated fat and high-cholesterol fed streptozotocin/nicotinamide diabetic rat model
- Marina Hernández-Martín 23
-
Aránzazu Bocanegra
12
-
Alba Garcimartín
12
- Jousef Ángel Issa 3
-
Rocío Redondo-Castillejo
12
-
Adrián Macho-González
24
-
Juana Benedí
12
-
Francisco José Sánchez Muniz
24
-
María Elvira López-Oliva
23
- 1 Department of Pharmacology, Pharmacy School, Complutense University of Madrid, Madrid, Spain
- 2 AFUSAN Group, Sanitary Research Institute of the San Carlos Clinical Hospital (IdISSC), Madrid, Spain
- 3 Departmental Section of Physiology, Pharmacy School, Complutense University of Madrid, Madrid, Spain
- 4 Department of Nutrition, Pharmacy School, Complutense University of Madrid, Madrid, Spain
Argitaletxea: Elsevier
ISBN: 9780443222399
Argitalpen urtea: 2024
Orrialdeak: 165-195
Mota: Liburuko kapitulua
Laburpena
The mucosal surface of gastrointestinal tract is lined with epithelial cells that establish an effective barrier between the lumen and internal environment through intercellular junctions, preventing the passage of potentially harmful substances. The “intestinal barrier function” consist of a defensive system that prevent the passage of antigens, toxins, and microbial products, while maintains the correct development of the epithelial barrier, the immune system and the acquisition of tolerance toward dietary antigens and intestinal microbiota. Intestinal morphology changes subsequent to nutritional variations, stress, aging or diseases, which can also affect the composition of the microbiota, altering the homeostasis of the intestine. A growing body of evidence suggests that alterations in intestinal barrier function favor the development of exaggerated immune responses, leading to metabolic endotoxemia, which seems to be the origin of many chronic metabolic diseases such as type 2 diabetes mellitus (T2DM). Although the mechanisms are still unknown, the interaction between dietary patterns, gut microbiota, intestinal mucosa, and metabolic inflammation seems to be a key factor for the development of T2DM, among other diseases. This chapter details the different techniques that allow evaluating the morphological and molecular alterations that lead of the intestinal barrier dysfunction in a T2DM experimental model. To induce both diabetic metabolic disturbances and gut barrier disruption, Wistar rats were fed a high-saturated fat and high-cholesterol diet and received a single dose of streptozotocin/nicotinamide. This animal model may contribute to clarify the understanding of the role of intestinal barrier dysfunction on the late-stage T2DM etiology.