Gene/Protein
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Pivot Concepts:
Gene/Protein
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Target Concepts:
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Query: EC:3.2.1.26 (
invertase
)
4,927
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
It has been shown previously that insulinlike growth factors (IGFs) stimulate the proliferation of intestinal crypt cells in vitro. To examine the in vivo effects of IGF-I on mucosal adaptation, three groups of Sprague-Dawley rats underwent 80% jejunoileal resection. Miniosmotic pumps were then inserted under the skin immediately after resection to deliver vehicle (resected control), 1.5 mg/kg per day of IGF-I, or 1.5 mg/kg per day of des-(1-3)-IGF-I (des-IGF-I). Des-IGF-I is a truncated form of IGF-I that binds as well to type I IGF receptors but less tightly to several forms of IGF-binding proteins (IGFBPs) than IGF-I. Ad libitum food intake did not differ among the three resected groups. Body weight gains were greater in animals receiving des-IGF-I than in those receiving IGF-I, which were greater than resected controls. All animals were killed 7 days postoperatively, and the remaining small intestine was removed and divided at the anastomotic site. Both IGF-I and des-IGF-I induced hyperplasia (increased DNA and protein content) in the duodenojejunum but not in the ileum. IGF-I and des-IGF-I were equally active. In contrast,
sucrase
, maltase, and leucine aminopeptidase activities were greater only in the ileum of animals receiving IGF-I and des-IGF-I than in resected controls. Although more potent in stimulating overall body weight gain, des-IGF-I was not more potent than IGF-I when duodenal and ileal responses were determined. IGF infusion (IGF-I greater than des-IGF-I) increased the levels of circulating IGFBP-3 and
IGFBP-2
, which may act to modulate the biological effectiveness of the infused peptides. These results suggest that both IGF-I and des-IGF-I may have potential as therapeutic agents for short bowel patients.
...
PMID:Truncated and native insulinlike growth factor I enhance mucosal adaptation after jejunoileal resection. 137 79
Proliferation and differentiation of rat (IEC-6) and human (FHs) small intestinal cells in the presence of epidermal growth factor (EGF), insulin, insulin-like growth factor (IGF)-I, -II, and des[1-3]tripeptide-IGF-I(des-IGF-I) were examined. Thymidine incorporation into IEC-6 cells was significantly increased by insulin, IGF-I, des-IGF-I, IGF-II, and IGF-I+EGF, but not by EGF alone. In contrast, thymidine incorporation into FHs cells was increased only by insulin, IGF-I, and the combination of IGF-I and EGF. Mitogenic activities of IGF-I at 5 nM and insulin at 700 nM (IEC-6) or 1400 nM (FHs) were equivalent, suggesting that both acted through the type I IGF receptor in both cells. IEC-6 cells secreted consistently one predominant IGF binding protein (IGFBP) with M(r) of 28.5 kDa, while FHs cells secreted several IGFBPs with M(r) from 43 to 24 kDa. Mitogenic activity of IGF-I at 5 nM was equal to des-IGF-I at 0.005 nM, indicating that endogenously produced IGFBPs likely inhibit IGF-I action. In IEC-6 cells,
IGFBP-2
secretion, but not mRNA expression, was decreased by EGF and IGF-I+EGF treatments, suggesting post-transcriptional regulation. IGF-II and EGF were more potent than IGF-I at increasing maltase and
sucrase
activities, suggesting that these growth factors may stimulate differentiation to a greater degree than mitogenesis.
...
PMID:Effects of insulin, insulin-like growth factors and epidermal growth factor on mitogenesis and disaccharidase activity in rat (IEC-6) and human (FHs 74 Int) intestinal cells. 905 10
The mechanisms which regulate cell turnover in the intestinal epithelium are incompletely understood. The present study was performed to characterize the role of autocrine IGF system components in intestine epithelial cell proliferation and differentiation comparing rapidly growing crypt cells (IEC-6) with differentiating enterocytes (CaCo-2). The autocrine release of IGF-I, IGF-II and IGFBP-1 through -3 was determined by specific RIAs and western ligand blotting. In addition, binding and growth-promoting activity of insulin, IGF-I and IGF-II was investigated. Enterocytic differentiation was assessed by measuring the brush-border enzymes alkaline phosphatase and
sucrase
. During IEC-6 growth, the autocrine release of IGF-I and -II increased, whereas
IGFBP-2
levels decreased. Specific receptors for IGF-I and IGF-II but not insulin could be detected. IGF-I was 100-fold more potent than insulin to stimulate IEC-6 cell proliferation. In contrast, CaCo-2 cells revealed higher binding of insulin than IGF-I/-II and no release of IGF-I. At switch from CaCo-2 cell proliferation to differentiation a marked increase in the secretion of IGF-II (10-fold), IGFBP-1 (2.5-fold),
IGFBP-2
(3-fold), and IGFBP-3 (6-fold) was measured. Our data indicate that IGF system components differentially modulate enterocytic cell proliferation and differentiation.
...
PMID:Differential autocrine regulation of intestine epithelial cell proliferation and differentiation by insulin-like growth factor (IGF) system components. 1022 88