Surgical Research Review| Volume 149, ISSUE 5, P601-605, May 2011

Acute “adaptation” by the small intestinal enterocyte: A posttranscriptional mechanism involving apical translocation of nutrient transporters

      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.
      • Secor S.M.
      • Diamond J.
      Adaptive responses to feeding in Burmese pythons: pay before pumping.
      Indeed, 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.
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