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Review
. 2012 Jun;41(2):409-23, vii.
doi: 10.1016/j.ecl.2012.04.018. Epub 2012 May 15.

Insulin-like growth factors in the gastrointestinal tract and liver

John F Kuemmerle  1
Affiliations
Review

Insulin-like growth factors in the gastrointestinal tract and liver

John F Kuemmerle. Endocrinol Metab Clin North Am. 2012 Jun.

Abstract

The liver is a major source of insulin-like growth factors (IGFs) and IGF binding proteins (IGFBPs) that are present in the circulation and have important endocrine activities relating to energy metabolism, body size, carcinogenesis, and various organ-specific functions. Although IGFs have only minor effects on the normal liver itself, production of IGFs and IGFBPs in a tissue-specific manner in the gastrointestinal tract exert important regulatory effects on cellular proliferation, survival, and apoptosis. IGFs and IGFBPs play important regulatory roles in the response of both the liver and the gastrointestinal tract to inflammation and in the development of neoplasia.

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Figures

Figure 1
Figure 1
Signaling cascades activated by the activated IGF-I receptor. The IGF-I receptor is located on the basolateral membrane of intestinal epithelial cells and on smooth muscle cells. Ligand binding and activation of the IGF-I receptor elicts phosphrylation of cytoplasmic tyrosine residues in this receptor tyrosine kinase. Subsequently binding of scaffolding and docking proteins results in activation of distinct intracellular signaling cascades that regulate proliferation and survival and collagen IαI expression.
Figure 2
Figure 2
Positive feedback between IGFBP-5 and IGF-I. The expression and effects of IGF-I and IGFBP-5 are linked whereby IGF-I stimulates IGFBP-5 expression and IGFBP-5, independent of IGF-I, stimulates IGF-I expression each reinforcing the expression and effects of the other.
Figure 3
Figure 3
Inflammation-induced fibrosis is decreased in IGF-I(+/−) mice. Collagen deposition in smooth muscle layer of vehicle-treated IGF-I(+/−) mice and its increase in response to TNBS-induced colitis are lower than in wildtype C57BL/6J mice.
Figure 4
Figure 4
Inflammation-induced collagen IαI expression is decreased in IGF-I(+/−) mice. Collagen IαI transcripts in smooth muscle cells of vehicle-treated IGF-I(+/−) mice and its increase in response to TNBS-induced colitis are lower than in wildtype C57BL/6J mice. Transcript levels were measured by real-time PCR using the 2−ΔΔCt method.
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