Is a normally functioning gastrointestinal tract necessary for normal growth in late gestation?

Blakelock, R. T.; Upadhyay, Vipul; Kimble, Roy M.; Pease, P. W. B.; Kolbe, Anne; Harding, Jane E.

doi:10.1007/s003830050234

Cited by 38 publications

(17 citation statements)

References 21 publications

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“…Nonetheless, because of increased size of the small intestine with increasing fetal age, the total small intestinal OAT enzymatic activity of the fetus steadily increases with fetal age. It has been suggested that the small intestine of fetal humans and rabbits is an important source of enteral nutrition for somatic growth and development (22,23). The fetal porcine small intestine may play a similar role, and this may be especially important at d 60 and thereafter, when the intestinal epithelium possesses absorptive and digestive capacities greater than those at earlier stages of gestation (24,25) and is able to absorb amino acids from swallowed amniotic fluid.…”

Section: Oat In Fetal Pig Small Intestinementioning

confidence: 99%

Ornithine Aminotransferase Messenger RNA Expression and Enzymatic Activity in Fetal Porcine Intestine

Dekaney

Jaeger

2001

Pediatr Res

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In most neonatal animals, the small intestinal epithelium is responsible for endogenous arginine production. The ability of neonatal enterocytes to synthesize arginine immediately after birth suggests that the enzymes involved are present prenatally. Pyrroline-5-carboxylate is the common intermediate in the intestinal pathways for the synthesis of citrulline and arginine from both glutamine and proline and is interconverted into ornithine by ornithine aminotransferase (OAT). In this study, OAT enzymatic activity and mRNA expression in the intestine of fetal pigs from 30 to 110 d of gestation were determined. Enzymatic activity (nanomoles per minute per milligram of protein) peaked at d 45 of gestation and increased again between d 60 and 110 of gestation. At 30 and 35 d of gestation, OAT mRNA expression was detected throughout the mucosal epithelium of the small intestine. Throughout the remainder of gestation, OAT expression was notably higher in the villus epithelium than in the crypt epithelium. The presence of OAT in the small intestinal epithelium throughout gestation suggests that the porcine small intestine is capable of interconverting ornithine and pyrroline-5-carboxylate during fetal development. This capability may be important for synthesis of arginine, proline, ornithine, and polyamines for development and metabolic activity of the intestine during gestation or for somatic growth of the fetus. Milk of many species, including human, cow, and pig, is relatively deficient in arginine (1). Additionally, arginine requirements by neonates are particularly high, partly because of arginine abundance in the body and multiple metabolic pathways for arginine utilization (2). Arginine is used for synthesis of proteins, polyamines, creatinine, and nitric oxide (3). Thus, endogenous synthesis of arginine must play an important role in arginine provision to the breast-fed neonate (3), and development of the intestinal arginine synthetic pathway before parturition is of crucial importance for neonatal survival and growth.Both enzymologic and metabolic studies have established that enterocytes of the small intestine synthesize citrulline and arginine from glutamine and proline ( Fig. 1) and are the major site for endogenous synthesis of arginine in neonates (2). OAT (EC 2.6.1.13) interconverts P-5-C and ornithine; P-5-C is the common intermediate in the intestinal pathways for the synthesis of citrulline and arginine from both glutamine and proline (Fig. 1). Thus, OAT plays an essential role in intestinal synthesis of citrulline and arginine. Consistent with this notion, hypoornithinemia, hypocitrullinemia, and hypoargininemia occur in OAT-deficient infants (4) and neonatal pigs (5), as well as in OAT-gene knockout newborn mice (4). The severity of OAT deficiency varies among species, and associated pathologic conditions are not realized until after birth. In OAT knockout mice OAT deficiency is lethal in neonates (4). In humans, OAT deficiency normally remains undetected until retinal degeneration associated with gy...

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Section: Oat In Fetal Pig Small Intestinementioning

confidence: 99%

Ornithine Aminotransferase Messenger RNA Expression and Enzymatic Activity in Fetal Porcine Intestine

Dekaney

Jaeger

2001

Pediatr Res

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“…Babies with upper gut atresias are at high risk of being born small for gestational age (Cozzi & Wilkinson 1969, Jolleys 1981, Pierro et al 1987. Babies with congenital gut anomalies are also proportionately smaller if they are born at term than if they are born preterm (Gitlin et al 1972, Pierro et al 1987, Blakelock et al 1998.…”

Section: Introductionmentioning

confidence: 99%

Enteral IGF-I enhances fetal growth and gastrointestinal development in oesophageal ligated fetal sheep

Kimble¹,

Breier²,

Gluckman³

et al. 1999

Journal of Endocrinology

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Infants with upper gut atresia often have impaired intrauterine growth and gut function. IGF-I is important in fetal growth and is contained in amniotic fluid. We therefore wanted to test the hypothesis that IGF-I infused into fetal gut would reverse the effects of an upper gut obstruction on gut structure and growth in fetal sheep.At 90 days gestation fetuses (n=6 per group) underwent oesophageal ligation, followed by continuous infusion of IGF-I (1-8 µg/day) or saline into the gut beyond the ligation until 137 days. Controls underwent sham ligation only. Oesophageal ligation tended to reduce fetal body and organ weights. IGF-I treatment prevented this reduction and increased body length and spleen weight above those of controls. The decrease in bowel wall thickness induced by oesophageal ligation was also prevented by IGF-I treatment. Amniotic fluid IGF-I concentrations did not change over gestation and were higher in the IGF-I treated group. No change in fetal plasma IGF-I concentrations were detectable. We conclude that enterally administered IGF-I may enhance fetal growth and gut development in utero and that IGF-I in amniotic fluid may play a physiological role in gut development in the fetus.

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“…During the last trimester human fetuses swallow fluid (up to 750 mL d Ϫ1 ) that contains dilute concentrations of protein, free amino acids, and a variety of growth factors (5-7) derived from amniotic fluid and lung and nasal secretions. Although nutrients absorbed from these fluids are estimated to provide 10 -15% of fetal nitrogen requirements (8), and congenital intestinal atresia in humans is associated with fetal growthretardation (9,10), it remains unclear whether the swallowed fluid is particularly important for the final phases of fetal GIT development. Evidence from humans and experimental animals (sheep, rabbits) suggests that esophageal obstruction may impair growth of the intestine, particularly if obstruction is complete and prevents luminal input in the final stage of gestation (9 -17).…”

mentioning

confidence: 99%

Prenatal Development of Gastrointestinal Function in the Pig and the Effects of Fetal Esophageal Obstruction

Sangild¹

2002

Pediatric Research

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Maturation of the fetal gastrointestinal tract (GIT) is influenced by both luminal stimuli (e.g. swallowed fluid) and hormonal factors (e.g. endogenous cortisol release). The aims of the present study were 1) to investigate GIT growth and maturation during the last 20% of gestation in pigs (term ϭ 114 Ϯ 2 d), and 2) to investigate the effect of esophageal ligation, to prevent fetal swallowing, at 80% to 91% gestation. In normal fetuses, marked increases occurred during late gestation in body weight (ϩ95%), relative intestinal weight (ϩ79%, g kg Ϫ1 body weight), activity of some digestive enzymes (1.5-to 10-fold), and absorption of glucose and intact proteins (3-to 6-fold). Fetuses with ligated esophagi had lowered body weight (Ϫ20%), reduced intestinal weight (Ϫ43%), aminopeptidase A activity (Ϫ24%), and glucose absorption (Ϫ27%), while lactase, sucrase, and dipeptidylpeptidase IV activities were increased (ϩ40 -50%), compared with sham-operated fetuses (all p Ͻ 0.05). Other parameters of GIT function remained unchanged by esophageal obstruction (absorption of amino acids and immunoglobulin, activity of chymosin, amylase, trypsin, chymotrypsin, maltase, aminopeptidase N -all expressed per gram GIT tissue). Ligated fetuses had elevated cortisol levels, which is known to stimulate fetal GIT maturation. We conclude that the rapid development of GIT function in late gestation is diminished by esophageal obstruction, mainly due to slower GIT growth and not inhibition of normal functional development of enterocytes. In many species, organ maturation is particularly rapid during the perinatal period. Development of the gastrointestinal tract (GIT) is stimulated by the transition from mainly parenteral nutrition before birth (via the placenta) to exclusively enteral nutrition after birth. Hence, enteral intake of nutrients in newborns elicits structural and functional GIT changes although the responses vary among species, source of nutrients, and specific GIT functions (1-4).Enteral nutrient intake may also play a role before birth. During the last trimester human fetuses swallow fluid (up to 750 mL d Ϫ1 ) that contains dilute concentrations of protein, free amino acids, and a variety of growth factors (5-7) derived from amniotic fluid and lung and nasal secretions. Although nutrients absorbed from these fluids are estimated to provide 10 -15% of fetal nitrogen requirements (8), and congenital intestinal atresia in humans is associated with fetal growthretardation (9, 10), it remains unclear whether the swallowed fluid is particularly important for the final phases of fetal GIT development. Evidence from humans and experimental animals (sheep, rabbits) suggests that esophageal obstruction may impair growth of the intestine, particularly if obstruction is complete and prevents luminal input in the final stage of gestation (9 -17). The GIT matures relatively early in primates, particularly when compared with laboratory rodents (18). Hence, studies of GIT maturation in species with longer gestation, such as the pig or shee...

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Is a normally functioning gastrointestinal tract necessary for normal growth in late gestation?

Cited by 38 publications

References 21 publications

Ornithine Aminotransferase Messenger RNA Expression and Enzymatic Activity in Fetal Porcine Intestine

Ornithine Aminotransferase Messenger RNA Expression and Enzymatic Activity in Fetal Porcine Intestine

Enteral IGF-I enhances fetal growth and gastrointestinal development in oesophageal ligated fetal sheep

Prenatal Development of Gastrointestinal Function in the Pig and the Effects of Fetal Esophageal Obstruction

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