Gastrointestinal Tract - Postnatal
- 1 Introduction
- 2 Some Recent Findings
- 3 Small Intestine Length
- 4 Lipid Signalling
- 5 Insulin-like Growth Factors
- 6 Gut Microorganism Population
- 7 Meconium
- 8 Abnormalities
- 9 References
- 10 Glossary Links
This page is an introduction to postnatal gastrointestinal tract development. This nutritionally involves a change from prenatal placental vascular nutrition to postnatal oral colostrum/milk enteral nutrition (enteral = nutritient delivery as fluid into the gastrointestinal tract). Also look at the topic of Milk in relationship to neonatal nutrition. The postnatal gastrointestinal tract development is also about increased activity of the tract and associated organs as well as the populating with intestinal flora in the tract. This is also the pathway for initial passive immunity through absorption of maternal immunoglobulin from breast milk.
Some Recent Findings
Small Intestine Length
Small intestine growth in length prenatally is initially linear during the first half pregnancy (to 32 cm CRL), followed by rapid growth in the last 15 weeks doubling the overall length.
Postnatally, growth continues rapidly but after 1 year slows again to a linear increase to adulthood.
|Age (weeks gestational age)||Average Length (cm)|
|1 year postnatal||380|
Table data based upon 8 published reports of necropsy measurement of 1010 guts.
- Links: Intestine Development
Lipids present in the intestine leads to a reduction in nutrient intake. Recent research has shown that lipids present in the intestine can also regulate endogenous nutrient production.
Signalling pathway: presence of ingested lipids - intestinal lipid sensors - signal to the brain - liver - reduction in endogenous glucose production
Insulin-like Growth Factors
Some evidence to suggest that in preterm infants IGFBP-2 and IGF-II present in breast milk may have an important role in their early development.
- insulin-like growth factors (IGFs) and IGF binding proteins (IGFBPs)
Gut Microorganism Population
The normal newborn gastrointestinal tract contains little if any microorganisms (commensal intestinal microbiota, microbiota, flora, microflora).
Postnatally, the tract has to be populated by microorganisms, which are mainly anaerobic bacteria and then aerobic bacteria, but may also include yeast and fungi. The foregut comparatively has few microorganisms when compared to the midgut and hindgut.
There are several infectious pathogens that can populate the postnatal gut leading to a number of different diseases: Escherichia coli (enterotoxigenic), Shigella (a gram-negative, non-spore forming rod-shaped bacteria infectious through poor hygeine and ingestion, fecal–oral contamination. More? Dysentery), Vibrio cholerae and Listeria.
Antibiotics - Treatment of other neonatal infections systemically with antibiotics can alter the bacterial population.
As introduced in fetal development, meconium is formed from gut and associated organ secretions as well as cells and debris from the swallowed amniotic fluid. Meconium accumulates during the fetal period in the large intestine (bowel). It can be described as being a generally dark colour (green black) , sticky and odourless.
- In fetal development, meconium is formed from gut and associated organ secretions as well as cells and debris from the swallowed amniotic fluid.
- Meconium accumulates during the fetal period in the large intestine (bowel).
- It can be described as being a generally dark colour (green black) , sticky and odourless.
Normally this meconium is defaecated (passed) postnatally over the first 48 hours and then transitional stools from day 4.
Abnormally this meconium is defaecated in utero, due to oxygen deprivation and other stresses.
Meconium Aspiration Syndrome
- Premature discharge into the amniotic sac can lead to mixing with amniotic fluid and be reswallowed by the fetus.
- This is meconium aspiration syndrome and can damage both the developing lungs and placental vessels.
- Absence or delayed passage of meconium may indicate conditions associated with meconium plugs or more seriously, Hirshsprung's disease (aganglionic colon, megacolon).
- Delayed conversion to transitional stools may indicate a feeding issue.
There are several infectious pathogens that can populate the postnatal gut leading to a number of different diseases:
- Escherichia coli (enterotoxigenic)
- Shigella a gram-negative, non-spore forming rod-shaped bacteria infectious through poor hygeine and ingestion, fecal–oral contamination. (More? Dysentery)
- Vibrio cholerae
- Links: Bacterial Infection
- (NEC) is a disease affecting infants born prematurely (mortality rate of 15-30%)
- up to 40% of afflicted premature infants require intestinal resection
- usually occurs in the second week of life after the initiation of enteral feeds
- pathogenesis is multifactorial
- appears to involve an overreactive response of the immune system to an insult.
- increased intestinal permeability, bacterial translocation, and sepsis.
|Neonate (human) necrotizing enterocolitis bacteria colonizing intestinal tissue.||Mouse model analysis of colonic microbiota. Mice with NEC (a) are compared to mice without NEC (b). * indicates statistically significantly more in mice with NEC. ** indicates statistically significantly more in mice without NEC.|
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Cite this page: Hill, M.A. (2020, October 31) Embryology Gastrointestinal Tract - Postnatal. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Gastrointestinal_Tract_-_Postnatal
- © Dr Mark Hill 2020, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G