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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)

To facilitate the study of regulators of differentiation and proliferation of small intestinal epithelium in the suckling rat we have developed a serum-free organ culture system and used it to examine epithelial responsiveness to various regulatory hormones. These hormones included the insulin-like growth factors (IGFs) whose action can be blocked by binding proteins in serum. Jejunal explants from 5-day-old suckling rats maintained better brush border enzyme activity and better histology when cultured under hyperbaric conditions for 24 h in serum-free Dulbecco's modified Eagle's medium/F12 medium than in RPMI 1640 plus 10% fetal bovine serum. Tissue responsiveness to various regulatory hormones was then tested in the serum-free medium. Insulin had no significant effect on morphology, proliferation rate, or enzyme activity in 5-day explants after 24 h in culture. However, insulin did increase lactase activity and induce the early appearance of sucrase in 10- and 12-day explants after 48 h in culture. Dexamethasone increased specific activities of alkaline phosphatase (30%, P < 0.001) and lactase (15%, P < 0.001), and reduced shedding of alkaline phosphatase into the medium (P < 0.001), in explants of 5-day-old rats cultured over 24 h. Dexamethasone combined with insulin had no obvious effect on the rate of protein or DNA synthesis but did increase villus height (P = 0.04) and crypt depth (P = 0.001) and acted synergistically to further increase lactase activity above levels obtained by either alone. IGF-I and IGF-II, des-(1-3)IGF-I, fibroblast growth factor (FGF), and growth hormone (GH) had no effect on morphology or biochemical activity of explants after 24 or 48 h culture.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum-free organ culture of suckling rat jejunum: effect of regulatory hormones. 795 13

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.
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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 effect of orally administered IGF-I on intestinal development was assessed in piglets. Cesarean-derived, colostrum-deprived piglets received formula alone or formula containing 65 nM (500 microg/L) of recombinant human IGF-I. IGF-I intake averaged 200 microg/kg/d. On d 7 and 14 postpartum, piglets were killed, organs were removed and weighed, and tissue and blood samples were collected. The small intestine was divided into 13 segments that were weighed and measured. A sample of each segment was fixed in formalin, and the mucosa was scraped for enzyme analyses. Food intake, body and organ weights, intestinal weight, length, protein, DNA and RNA content did not differ between the treatment groups. Serum IGF-I, IGF-II, and IGF-binding protein profiles and tissue IGF-binding protein mRNA expression were also comparable between the treatment groups. In contrast, intestinal enzymes and villus height were increased by oral IGF-I. Lactase was approximately 2-fold higher (p < or = 0.05) in the jejunum and proximal ileum, and sucrase was approximately 50% higher (p < or = 0.05) in the jejunum of IGF-I-treated animals than in controls. Villus height in the terminal ileum was approximately 50% greater in IGF-I-treated animals than in controls (p = 0.03). In conclusion, orally administered IGF-I at 200 microg/kg did not affect whole body or organ growth or serum IGF-I concentrations; however, intestinal disaccharidase activity and ileal villus growth were responsive to orally administered IGF-I, supporting a potential role for milk-borne IGF-I in neonatal intestinal development.
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PMID:Small intestinal disaccharidase activity and ileal villus height are increased in piglets consuming formula containing recombinant human insulin-like growth factor-I. 921 41

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.
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PMID:Differential autocrine regulation of intestine epithelial cell proliferation and differentiation by insulin-like growth factor (IGF) system components. 1022 88