Linked Life Data

19524295

Source:http://linkedlifedata.com/resource/pubmed/id/19524295

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2009-7-28
pubmed:abstractText
The function of glycogen in the placenta remains controversial. Whether it is used as a source of fuel for placental consumption or by the fetus in times of need has yet to be determined. Two imprinted genes, insulin-like growth factor 2 (Igf2) and H19 are highly expressed in the placenta. We have previously demonstrated that mice with Igf2 deficiency have lower levels of placental glycogen. In this study, we used mice with targeted disruption of the H19 gene (H19(-/-)) to determine the importance of Igf2 over-expression in placental growth and glycogen stores. In addition, since Igf2 mediates most of its functions by signaling through the insulin and/or IGF Type 1 receptors, we determined whether gene deletions to these receptors could affect placental glycogen stores. Our data demonstrate that placentas from H19(-/-) mice are heavier, have higher number of glycogen cells, and contain larger glycogen concentrations than those of H19(+/+) mice. No differences in GSK-3, ERK, or total Akt expression or phosphorylation were found between genotypes; however, Akt1 protein expression levels were significantly increased in H19(-/-) placentas. Results obtained from insulin receptor or IGF Type 1 receptor mutant mice did not show differences in placental glycogen content compared to their wild-type littermates, supporting the notion of a specific placental Igf2 receptor. Taken together, these results support a role for Igf2 and Akt1, but not the insulin nor the IGF Type 1 receptors, in the regulation of placental growth and glycogen metabolism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1532-3102
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
693-9
pubmed:dateRevised
2011-10-7
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Placental glycogen stores are increased in mice with H19 null mutations but not in those with insulin or IGF type 1 receptor mutations.
pubmed:affiliation
Endocrine Division, Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural