Intestinal Adaptation

The intestine contains a perpetually proliferating and differentiating epithelium that gives it the ability to regenerate and adapt to the loss of functional surface area. (1)

When considering the possibility of intestinal adaptation, it is important to understand the normal physiology of the intestine. On a regular basis, the entire small intestine epithelium is replaced every 3-5 days. The regenerative capacity of the small intestine is based upon the activity of the epithelial stem cells that are found within the base of the epithelial crypts. (1)

When a person undergoes intestinal resection, the intestine undergoes adaptations in order to try and continue to support the nutritional state of the person. Evidence for functional adaptation in patient’s include the observation that parenteral fluid and electrolyte requirements decline with time after resection and many patients can be weaned from TPN. (1)

The intestinal adaptive response is characterized by:

• Crypt cell hyperplasia- crypt cell proliferation is increased after partial resection of the proximal small intestine

• Villus lengthening- villus hyperplasia occurs, villi are longer, there are increased numbers of all 4 differentiated cells types

• Increased absorptive function

The ability to survive free of parenteral nutrition support following intestinal resection depends on the residual functional intestinal capacity, the compensatory mechanisms of the remaining intestine, and the adaptive restoration.

Humoral Mediators (2)

Glucagon Like Peptide-2 (GLP-2)

• Intestine specific 33 amino acid peptide product of the post-translational processing of proglucagon

• Produced by the L cells in the ileum and colon

• Produced when there are luminal nutrients in the ileum and/or colon

• Enhances small and large intestinal villus and crypt cell growth

• Helps to maintain mucosal integrity

• Helps to increase nutrient absorption

• Teduglutide, a GLP-2 analog, has recently been approved as an agent to use in patients with short bowel syndrome to improve intestinal absorption

Neurotensin

• Produced by N cells in the jejunum and ileum

• Stimulated by luminal fats in the proximal small intestine

• Reduces gastric acid secretion and gastrointestinal motility

• Stimulates pancreatic bicarbonate secretion

Peptide YY

• Produced by L cells in the ileum and colon

• Stimulated by lipids, proteins, fatty acids, bile salts, cholecystokinin, and gastric acids

• Slows gastric emptying and small bowel motility

• Promotes satiety

• Reduces gastric acid secretion and intestinal fluid secretion

To learn more about the pathophysiology in short bowel syndrome, please review this article.

References:

1. Langnas AN, Goulet O, Quigley EMM, Tappenden KA. Intestinal Failure Diagnosis, Management, and Transplantation. Malden, MA: Blackwell; 2008.

2. Tappenden KA. Pathophysiology of Short Bowel Syndrome. Journal of Parenteral and Enteral Nutrition. 2014;38(1_suppl). doi:10.1177/0148607113520005.