Investigation of Three Doses of Oral Insulin-like Growth Factor-I on Jejunal Lactase Phlorizin Hydrolase Activity and Gene Expression and Enterocyte Proliferation and Migration in Piglets

Houle, Vicki M.; Park, Yoo Kyoung; Laswell, Stacy C; Freund, Gregory G.; Dudley, Mary A.; Donovan, Sharon M.

doi:10.1203/00006450-200010000-00013

Cited by 47 publications

(52 citation statements)

References 39 publications

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“…Serum IGF1 concentrations did not differ between replacer-fed pigs with or without supplemental IGF1 for 4 days from birth when evaluated at 24, 48, 72, or 96 h postnatal (Burrin et al 1996). Similarly, porcine serum IGF1 concentrations assessed on PND14 were unaffected by oral supplementation of IGF1 delivered in milk replacer (Houle et al 2000). Nevertheless, both studies reported proliferative effects in the GI tract for IGF1-supplemented pigs (Burrin et al 1996, Houle et al 2000.…”

Section: Discussionmentioning

confidence: 84%

“…Similarly, porcine serum IGF1 concentrations assessed on PND14 were unaffected by oral supplementation of IGF1 delivered in milk replacer (Houle et al 2000). Nevertheless, both studies reported proliferative effects in the GI tract for IGF1-supplemented pigs (Burrin et al 1996, Houle et al 2000. By contrast, serum IGF1 concentrations in neonatal rats fed formula supplemented with IGF1 for 3 days were higher than those found in rats fed formula devoid of IGF1 (Philipps et al 1997).…”

Section: Discussionmentioning

confidence: 90%

“…euthanized at birth (nZ10), before nursing, nursed ad libitum from birth to PND2 (nZ7) or PND14 (nZ6), or gavage-fed milk replacer (30 ml/kg body weight (BW) per 2 h) from birth to PND2 (nZ5) or PND14 (nZ5). The milk replacer dosages followed published recommendations (Houle et al 2000). The cervices were collected on PND0, PND2, or PND14.…”

Section: Animalsmentioning

confidence: 99%

“…In the porcine neonate, a window for transmission of macromolecules, including MbFs, is open before gut closure, which is estimated to occur within 48 h of birth (Leece 1973). Orally administered IGF1 is locally bioactive in neonatal pigs, promoting intestinal crypt cell proliferation and increasing villus height (Xu et al 1994, Burrin et al 1996, Houle et al 2000. Whether oral IGF1 affects somatic tissue development beyond the gastrointestinal (GI) tract is unknown.…”

Section: Introductionmentioning

confidence: 99%

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Effects of age, nursing, and oral IGF1 supplementation on neonatal porcine cervical development

Camp¹,

Wiley²,

Boulos³

et al. 2014

Reproduction

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Nursing supports neonatal porcine uterine and testicular development, however, lactocrine effects on cervical development are undefined. Studies were conducted to determine the effects of i) age and the imposition of the lactocrine-null state from birth (postnatal day 0 (PND0)) by milk replacer feeding on cervical histology; ii) imposition of the lactocrine-null state for 2 days from birth on cervical cell proliferation, as reflected by proliferating cell nuclear antigen immunostaining; and iii) a single feeding of colostrum or milk replacer, administered at birth, with or without oral IGF1, on cervical cell proliferation and phosphorylated AKT (pAKT) and B-cell lymphoma 2 (BCL2) protein levels at 12 h postnatal. Cervical crypt depth and height of luminal epithelium (LE) increased with age by PND14, when both responses were reduced in replacer-fed gilts. Cell proliferation was reduced in LE at PND2, and in crypt epithelium and stroma by PND14 in replacer-fed gilts. Returning replacer-fed gilts to nursing on PND2 did not rescue the cervical phenotype by PND14. A single feeding of colostrum, but not milk replacer, was sufficient to support cervical cell proliferation at 12 h postnatal. IGF1 supplementation induced cell proliferation in replacer-fed gilts, and increased cervical pAKT and BCL2 levels in colostrum-fed gilts and replacer-fed gilts at 12 h postnatal. Results indicate that age and nursing support porcine cervical development, support is initiated at first ingestion of colostrum, IGF1 may be lactocrine-active, and identification of lactocrine-active factors can be accomplished by 12 h postnatal using this bioassay system.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 90%

Section: Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effects of age, nursing, and oral IGF1 supplementation on neonatal porcine cervical development

Camp¹,

Wiley²,

Boulos³

et al. 2014

Reproduction

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“…To measure enterocyte migration, animals with established NEC or controls were injected with bromodeoxyuridine (50 mg/kg 5Ј-BrdUrd; Sigma) intraperitoneally and then sacrificed either 1 or 18 h later. Samples of terminal ileum were then immunostained using anti-BrdUrd antibodies as described (42). Enterocyte migration was expressed by 1) measuring the distance from the bottom of the crypt to the foremost labeled enterocyte and 2) expressing the distance as a percentage of total villus height.…”

Section: Determination Of Enterocyte Migration and Intestinalmentioning

confidence: 99%

Endotoxin Inhibits Intestinal Epithelial Restitution through Activation of Rho-GTPase and Increased Focal Adhesions

Çetin

Ford

Sysko

et al. 2004

Journal of Biological Chemistry

130

145

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Diseases of gut inflammation such as neonatal necrotizing enterocolitis (NEC) result after an injury to the mucosal lining of the intestine, leading to translocation of bacteria and endotoxin (lipopolysaccharide). Intestinal mucosal defects are repaired by the process of intestinal restitution, during which enterocytes migrate from healthy areas to sites of injury. In an animal model of NEC, we determined that intestinal restitution was significantly impaired compared with control animals. We therefore sought to determine the mechanisms governing enterocyte migration under basal conditions and after an endotoxin challenge. Here we show that the cytoskeletal reorganization and stress fiber formation required for migration in IEC-6 enterocytes requires RhoA. Enterocytes were found to express the endotoxin receptor Toll-like receptor 4, which served to bind and internalize lipopolysaccharide. Strikingly, endotoxin treatment significantly inhibited intestinal restitution, as measured by impaired IEC-6 cell migration across a scraped wound. Lipopolysaccharide was found to increase RhoA activity in a phosphatidylinositol 3-kinasedependent manner, leading to an increase in phosphorylation of focal adhesion kinase and an enhanced number of focal adhesions. Importantly, endotoxin caused a progressive, RhoA-dependent increase in cell matrix tension/contractility, which correlated with the observed impairment in enterocyte migration. We therefore conclude that endotoxin inhibits enterocyte migration through a RhoA-dependent increase in focal adhesions and enhanced cell adhesiveness, which may participate in the impaired restitution observed in experimental NEC.Necrotizing enterocolitis (NEC) 1 is the leading cause of death from gastrointestinal disease in neonates and is second to respiratory disease as the overall leading cause of morbidity and mortality in this population (1-3). Clinical manifestations of NEC include abdominal distention, feeding intolerance, and systemic sepsis, which result from the destruction of the intestinal barrier (4, 5). Mucosal breakdown may occur as a result of a perinatal insult, such as hypoxia, which allows bacteria and bacterial by-products to breach the normally impermeable mucosal barrier and initiate a local and systemic inflammatory response (4,6,7,9). This causes the release of proinflammatory cytokines, including tumor necrosis factor, platelet-activating factor, nitric oxide, and endotoxin, which lead to further epithelial injury (10 -13). Following mucosal damage, healing occurs initially through the process of epithelial restitution, in which healthy enterocytes adjacent to the sites of injury migrate toward the denuded mucosa to bridge the defect (14 -18). We hypothesize that the intestinal barrier defect in NEC does not result from epithelial injury alone but also from impaired restitution. This paper focuses specifically on the process of enterocyte migration, which is the sine qua non of epithelial restitution and mucosal healing.Although a variety of cytokines may be importan...

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Intestinal Protein and LPH Synthesis in Parenterally Fed Piglets Receiving Partial Enteral Nutrition and Enteral Insulinlike Growth Factor 1

Park,

Dudley,

Burrin

et al. 2001

J. pediatr. gastroenterol. nutr.

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BackgroundProviding partial enteral nutrition (PEN) supplemented with insulinlike growth factor‐1 (IGF‐1) to parenterally fed piglets increases lactase–phlorizin hydrolase (LPH) activity, but not LPH mRNA. The current aim was to investigate potential mechanisms by which IGF‐1 up‐regulates LPH activity.MethodsNewborn piglets (n = 15) received 100% parenteral nutrition (TPN), 80% parenteral nutrition + 20% parenteral nutrition (PEN), or PEN + IGF‐1 (1.0 mg · kg−1 · d−1) for 7 days. On day 7, [2H3]‐leucine was intravenously administered to measure mucosal protein and brush border LPH (BB LPH) synthesis.ResultsWeight gain, nutrient intake, and jejunal weight and length were similar among the treatment groups. Partial enteral nutrition alone increased mucosal weight, villus width and cross‐sectional area, LPH activity, mRNA expression, and high mannose LPH precursor (proLPHh) abundance compared with TPN (P <0.05). Insulinlike growth factor‐1 further increased mucosal weight, LPH activity, and LPH activity per unit BB LPH approximately twofold over PEN alone (P < 0.05) but did not affect LPH mRNA or the abundance of proLPHh (one of the LPH isoforms) or mature LPH. Isotopic enrichment of [2H3]‐leucine in plasma, mucosal protein, and LPH precursors, and the fractional and absolute synthesis rates of mucosal protein and LPH were similar among the treatment groups. Insulinlike growth factor‐1 treatment increased total mucosal protein synthesis (60%, P < 0.05) but not LPH synthesis compared with the other two groups.ConclusionsBecause IGF‐1 did not affect the fractional synthesis rate of either mucosal protein or LPH, the authors suggest that enteral IGF‐1 increases mucosal protein mass and LPH activity by suppressing mucosal proteolytic degradation.

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Investigation of Three Doses of Oral Insulin-like Growth Factor-I on Jejunal Lactase Phlorizin Hydrolase Activity and Gene Expression and Enterocyte Proliferation and Migration in Piglets

Cited by 47 publications

References 39 publications

Effects of age, nursing, and oral IGF1 supplementation on neonatal porcine cervical development

Effects of age, nursing, and oral IGF1 supplementation on neonatal porcine cervical development

Endotoxin Inhibits Intestinal Epithelial Restitution through Activation of Rho-GTPase and Increased Focal Adhesions

Intestinal Protein and LPH Synthesis in Parenterally Fed Piglets Receiving Partial Enteral Nutrition and Enteral Insulinlike Growth Factor 1

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