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Review
. 2016 May 14;2(4):429-438.
doi: 10.1016/j.jcmgh.2016.05.001. eCollection 2016 Jul.

The Pathogenesis of Resection-Associated Intestinal Adaptation

Brad W Warner  1
Affiliations
Review

The Pathogenesis of Resection-Associated Intestinal Adaptation

Brad W Warner. Cell Mol Gastroenterol Hepatol. .

Abstract

After massive small-bowel resection, the remnant bowel compensates by a process termed adaptation. Adaptation is characterized by villus elongation and crypt deepening, which increases the capacity for absorption and digestion per unit length. The mechanisms/mediators of this important response are multiple. The purpose of this review is to highlight the major basic contributions in elucidating a more comprehensive understanding of this process.

Keywords: Absorption; Adaptation; Angiogenesis; Apoptosis; EGF, epidermal growth factor; Epithelium; GH, growth hormone; GLP-2, glucagon-like peptide-2; Growth Factors; IGF-1, insulin-like growth factor-1; LA, lactate-accumulator; PN, parenteral nutrition; Proliferation; Rb, retinoblastoma protein; SBBO, small-bowel bacterial overgrowth; SBR, small-bowel resection; Villus.

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Figures

Figure 1
Figure 1
Factors that play a role in resection-induced intestinal adaptation.
Figure 2
Figure 2
Key signaling events that have been established to play a role in mechanisms for how EGF amplifies resection-induced intestinal adaptation. ERK, extracellular signal-regulated kinase.
See this image and copyright information in PMC

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