Effects of Intrauterine Growth on Intestinal Length in the Human Fetus

Shanklin, Douglas R.; Cooke, R. J.

doi:10.1159/000243974

Cited by 45 publications

(42 citation statements)

References 7 publications

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“…Previous studies also observed changes in the size and histopathology of the thymus in animal models of IUGR and stillborn infants (Lansdown 1977;D'Inca et al 2010c). Our findings agree with previous observations that also suggested that IUGR was associated with poorly developed SIs, which were shorter and thinner than those of normal piglets, although the relative length of the SI in IUGR was longer (Wang et al 2005;D'Inca et al 2010c;Shanklin and Cooke 1993). Michiels et al (2013) also reported maldevelopment of the digestive tract of the IUGR piglets in the post-weaning period.…”

Section: Discussionsupporting

confidence: 90%

Intrauterine Growth Restriction Impairs Small Intestinal Mucosal Immunity in Neonatal Piglets

Zhong

Ahmad

et al. 2014

J Histochem Cytochem.

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SummaryIntrauterine growth restriction (IUGR) is a very common problem in both piglet and human neonate populations. We hypothesized that IUGR neonates have impaired intestinal mucosal immunity from birth. Using neonatal piglets as IUGR models, immune organ weights, the weight and length of the small intestine (SI), intestinal morphology, intraepithelial immune cell numbers, levels of cytokines and immunoglobulins, and the relative gene expression of cytokines in the SI were investigated. IUGR neonatal piglets were observed to have lower absolute immune organ weight and SI length, decreased relative weights of the thymus, spleen, mesenteric lymph node, and thinner but longer SIs. Damaged and jagged villi, shorter microvilli, presence of autophagosomes, swelled mitochondria, and decreased villus surface areas were also found in the SIs of IUGR neonatal piglets. We also found a smaller number of epithelial goblet cells and lymphocytes in the SIs of IUGR neonates. In addition, we detected reduced levels of the cytokines TNF-α and IFN-γ and decreased gene expression of cytokines in IUGR neonates. In conclusion, IUGR was shown to impair the mucosal immunity of the SI in neonatal piglets, and the ileum was the major site of impairment. (J Histochem Cytochem 62:510-518, 2014)

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Section: Discussionsupporting

confidence: 90%

Intrauterine Growth Restriction Impairs Small Intestinal Mucosal Immunity in Neonatal Piglets

Zhong

Ahmad

et al. 2014

J Histochem Cytochem.

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“…This phenomenon could explain the reduction in intestinal development observed at birth in infants with IUGR (20) and some animal models of IUGR (21). IUGR impairs cell proliferation (22) and absorptive (23) and digestive (24) functions in small intestine.…”

mentioning

confidence: 93%

“…IUGR impairs cell proliferation (22) and absorptive (23) and digestive (24) functions in small intestine. It was found to produce alterations in colonic development, such as a reduction in colonic length or weight, or in the number of goblet cells in animal models of IUGR (20,25). Yet, the specific effect of IUGR on mucin gene expression and secretion has not been addressed.…”

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confidence: 99%

Intrauterine Growth Restriction Alters Postnatal Colonic Barrier Maturation in Rats

et al. 2009

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Intrauterine growth restriction (IUGR) is a leading cause of perinatal mortality and morbidity and increases the risk for necrotizing enterocolitis. We hypothesized that colonic barrier disruption could be responsible for intestinal frailty in infants and adults born with IUGR. Mucins and trefoil factor family 3 (TFF3) actively contribute to epithelium protection and healing. Our aim was to determine whether IUGR affects colonic mucosa maturation. IUGR was induced by dietary protein restriction in pregnant dams. Mucins and Tff3 expression and morphologic maturation of the colonic mucosa were followed during postnatal development of the offspring. Before weaning, mucin 2 and Tff3 protein levels were reduced in colonic mucosa of rats with IUGR compared with controls. After weaning, expression of mucin 2 (mRNA and protein) and mucin 4 (mRNA) were lower in colonic mucosa of rats with IUGR. At the same time, IUGR was associated with a reduction of crypt depth and a higher percentage of crypts in fission. We conclude that IUGR impairs mucus barrier development and is associated with long-term alterations of mucin expression. The lack of an efficient colonic barrier induced by IUGR may predispose to colonic injury not only in neonatal life but also in later life.

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“…ntestinal epithelial development changes immediately after birth, with an age-dependent enterocyte proliferation and differentiation pattern (1). Intestinal cell growth peaks at birth (2,3) upon the stimulation exerted by growth factors in amniotic fluid and in human milk (4,5), but also as a consequence of dietary changes (6).…”

mentioning

confidence: 99%

Lactoferrin Induces Concentration-Dependent Functional Modulation of Intestinal Proliferation and Differentiation

et al. 2007

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Human milk stimulates intestinal development through the effects of various moieties. Lactoferrin (LF) is a glycoprotein of human milk whose concentration is highest in colostrum decreasing in mature milk. LF promotes enterocyte growth in intestinal cell lines. We tested the hypothesis that LF induces a distinct effect on enterocyte proliferation and differentiation, depending on its concentration. We examined the dose-related effects by humannative LF (N-LF) in Caco-2 (human colon adenocarcinoma) cells. At high concentrations, N-LF stimulated cell proliferation in immature Caco-2 cells, as judged by 3 H-thymidine incorporation. In contrast, sucrase and lactase activities were increased at low but not high LF concentrations and their mRNA were also increased, indicating a transcriptional effect. Because iron binds specific LF sites, we compared the potency of N-LF and iron-saturated LF (I-LF) and found the native form more potent. Finally, we tested the effects by bovine LF (bLF) in the same system and found the latter more potent than the human isoform in inducing cell growth and lactase expression. These results suggest that LF directly induces enterocyte growth and proliferation, depending on its concentration, thereby regulating the earlyx postnatal intestinal development. bLF could be added to infant formula as a growth factor in selected intestinal diseases.

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Effects of Intrauterine Growth on Intestinal Length in the Human Fetus

Cited by 45 publications

References 7 publications

Intrauterine Growth Restriction Impairs Small Intestinal Mucosal Immunity in Neonatal Piglets

Intrauterine Growth Restriction Impairs Small Intestinal Mucosal Immunity in Neonatal Piglets

Intrauterine Growth Restriction Alters Postnatal Colonic Barrier Maturation in Rats

Lactoferrin Induces Concentration-Dependent Functional Modulation of Intestinal Proliferation and Differentiation

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