Linked Life Data

15525940

Source:http://linkedlifedata.com/resource/pubmed/id/15525940

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7020
pubmed:dateCreated
2004-12-23
pubmed:abstractText
At birth the trans-placental nutrient supply is suddenly interrupted, and neonates face severe starvation until supply can be restored through milk nutrients. Here, we show that neonates adapt to this adverse circumstance by inducing autophagy. Autophagy is the primary means for the degradation of cytoplasmic constituents within lysosomes. The level of autophagy in mice remains low during embryogenesis; however, autophagy is immediately upregulated in various tissues after birth and is maintained at high levels for 3-12 h before returning to basal levels within 1-2 days. Mice deficient for Atg5, which is essential for autophagosome formation, appear almost normal at birth but die within 1 day of delivery. The survival time of starved Atg5-deficient neonates (approximately 12 h) is much shorter than that of wild-type mice (approximately 21 h) but can be prolonged by forced milk feeding. Atg5-deficient neonates exhibit reduced amino acid concentrations in plasma and tissues, and display signs of energy depletion. These results suggest that the production of amino acids by autophagic degradation of 'self' proteins, which allows for the maintenance of energy homeostasis, is important for survival during neonatal starvation.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1476-4687
pubmed:author
pubmed:issnType
Electronic
pubmed:day
23
pubmed:volume
432
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1032-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The role of autophagy during the early neonatal starvation period.
pubmed:affiliation
Time's Arrow and Biosignaling, PRESTO, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't