Analysis of immunohistomorphological changes in the colonic mucosa in a high-saturated fat and high-cholesterol fed streptozotocin/nicotinamide diabetic rat model

  1. Marina Hernández-Martín 23
  2. Aránzazu Bocanegra 12
  3. Alba Garcimartín 12
  4. Jousef Ángel Issa 3
  5. Rocío Redondo-Castillejo 12
  6. Adrián Macho-González 24
  7. Juana Benedí 12
  8. Francisco José Sánchez Muniz 24
  9. María Elvira López-Oliva 23
  1. 1 Department of Pharmacology, Pharmacy School, Complutense University of Madrid, Madrid, Spain
  2. 2 AFUSAN Group, Sanitary Research Institute of the San Carlos Clinical Hospital (IdISSC), Madrid, Spain
  3. 3 Departmental Section of Physiology, Pharmacy School, Complutense University of Madrid, Madrid, Spain
  4. 4 Department of Nutrition, Pharmacy School, Complutense University of Madrid, Madrid, Spain
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Libro:
Methods in Cell Biology: Animal Models of Disease Part A

Editorial: Elsevier

ISBN: 9780443222399

Año de publicación: 2024

Páginas: 165-195

Tipo: Capítulo de Libro

DOI: 10.1016/BS.MCB.2024.02.010 GOOGLE SCHOLAR lock_openAcceso abierto editor

Resumen

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.