NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Rao JN, Wang JY. Regulation of Gastrointestinal Mucosal Growth. San Rafael (CA): Morgan & Claypool Life Sciences; 2010.

Cover of Regulation of Gastrointestinal Mucosal Growth

Regulation of Gastrointestinal Mucosal Growth.

Show details


The epithelium of mammalian gastrointestinal (GI) mucosa has the most rapid turnover rate of any tissue in the body, and maintenance of its integrity depends on a complex interplay between processes involved in cell proliferation, differentiation, migration, and apoptosis. Under physiological conditions, undifferentiated epithelial cells continuously replicate in the proliferating zone within the crypts and differentiate as they migrate up the luminal surface of the colon and the villous tips in the small intestine. To maintain stable numbers of enterocytes, cell division must be dynamically counterbalanced by apoptosis, a fundamental biological process involving selective cell deletion to regulate tissue homeostasis. Apoptosis occurs in the crypt area, where it maintains the critical balance in cell number between newly divided and surviving cells and at the luminal surface of the colon and villous tips in the small intestine, where differentiated cells are lost. This rapid dynamic turnover rate of the intestinal epithelium is highly regulated at different levels and is critically controlled by numerous factors.

Consistent with most other tissues in the body, the regulation of the growth of GI mucosa is unique and affected by the same hormones such as insulin, growth hormone, thyroxine, and cortisol that alter metabolism in other tissues. However, the GI mucosa also responds to a host of events triggered by the ingestion and presence of food within the digestive tract. Food directly interacts with the GI mucosa and results in the release of several gut hormones that specifically affect only tissues of the GI tract and regulate its growth. Compared with gut hormones, various factors theorized to affect the mucosa within the lumen are less well defined. These factors include secretions (especially those of the pancreas and liver), luminal nutrition, and additional dietary constituents that stimulate growth independent of their nutritive value. Although physiological significance of these factors remains to be fully investigated, the common property of these stimulants, which accounts for their scientific interest, is that they occur within the lumen, distributed over a proximal-to-distal gradient. These luminal factors are diluted, absorbed, and destroyed as they pass down the GI tract, therefore, their effects on the mucosa also decrease distally. Such a mechanism has been thought to explain the villous-height–crypt-depth gradient and a variety of adaptations that occurs after exposure of portions of the gut to luminal contents, such as GI bypass surgery.

In this chapter, we will give an overview of the new advance in the regulation of GI mucosal growth, particularly the involvement of intestinal stem cells in epithelial renewal and cellular signals that are activated during adaptation and control epithelial cell division and apoptosis. We also examine the trophic properties of a variety of gut peptides and luminal factors and some of the hypotheses invoked to explain the gradient-oriented nature of mucosal growth. Finally, to summarize part of the knowledge in the area, we review the roles of cellular polyamines in GI mucosal growth and analyze in some detail the mechanisms by which polyamines regulate expression of various growth-related genes at both transcription and posttranscription levels.

Copyright © 2011 by Morgan & Claypool Life Sciences.
Bookshelf ID: NBK54095


  • PubReader
  • Print View
  • Cite this Page

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...