The small intestine is an incredibly adaptable, “plastic” organ, the tissues of which are involved intimately in endocrine regulation, immune surveillance, multiple aspects of metabolism, excretion of metabolites, symbiosis with the enteric microbiome, and, of course, absorption of ingested nutrients. As the primary site of nutrient absorption, the gut must be adaptable to the quality, quantity, and timing of nutrient availability to optimize nutrient absorption and maintain health. Indeed, intestinal adaptation, as evident by changes in gene expression as the neonate grows older and transitions from breast milk to oral nutrients (ontogeny), is well described. Similarly, chronic changes in diet/nutrient supply alter gene expression resulting in different levels of nutrient transporters by the enterocytes. A dramatic example of this remodeling of the gut mucosa was demonstrated by Secor and Diamond in studying the onset of hyperplasia/hypertrophy in Burmese pythons in response to ingestion of a meal.
1Indeed, these forms of classic, genomic-mediated adaptation result in a change not only in function but also in structure of the mucosa, and typically occur over days. Similarly, when major parts of the intestinal absorptive surface area are lost (via resection for trauma, neoplasm, or disease) or bypassed (jejunoileal bypass), a remarkable hypertrophy/hyperplasia occurs, again through a complex set of changes in gene expression and cellular proliferation leading to villus hypertrophy and cellular hyperplasia.
- Secor S.M.
- Diamond J.
Adaptive responses to feeding in Burmese pythons: pay before pumping.
J Exp Biol. 1995; 198: 1313-1325
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- Adaptive responses to feeding in Burmese pythons: pay before pumping.J Exp Biol. 1995; 198: 1313-1325
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Accepted: February 10, 2011
AT is supported by a KL2 Medical Research Investigator Training (MeRIT) grant awarded via Harvard Catalyst | The Harvard Clinical and Translational Science Center (NIH grant #1KL2RR025757-01 and financial contributions from Harvard University and its affiliated academic health care centers). MGS has support from The Groff Foundation and NIH R01 DK39337.
© 2011 Mosby, Inc. Published by Elsevier Inc. All rights reserved.