Linked Life Data

16077193

Source:http://linkedlifedata.com/resource/pubmed/id/16077193

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2005-8-3
pubmed:abstractText
Apoptosis is a fundamental process in the development of the fast growing intestinal mucosa. Apoptotic cells are present along the whole length of the villi and in the crypts. The mechanisms involved in the induction of apoptosis in the gut mucosa are still unknown. Cytokines are believed to play a role in auto- and paracrine models because the cells are dying in so-called "packets" containing neighboring cells. In the rapidly developing gut of neonates, the apoptosis rate is transiently reduced in the first days of life, enhancing the growth of mucosa. Afterwards, apoptosis plays a role in the exchange of the enterocyte population, facilitating maturation of the mucosa. The presence of autophagic cells has been confirmed for the first time in the developing gut. Deprivation of growth factors during feeding artificial milk formula led to an increased apoptosis rate. Supplementation with leptin reduced cell apoptosis and increased the mitosis-to-apoptosis ratio. Autophagy was also diminished. The key to healthy gut mucosa growth in early life, especially in fast-growing animals, is colostrum, which supplies nutritional and defensive components together with supplementary growth factors, cytokines and hormones essential for growth and maturation of gut mucosa.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1899-1505
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
56 Suppl 3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7-24
pubmed:dateRevised
2008-5-19
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Into the unknown--the death pathways in the neonatal gut epithelium.
pubmed:affiliation
Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw Agricultural University, Warsaw, Poland. mickgodl@hotmail.com
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't