Linked Life Data

18056789

Source:http://linkedlifedata.com/resource/pubmed/id/18056789

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-2-8
pubmed:abstractText
Hepatic glucose production is normally activated at birth but has been observed in response to experimental hypoglycemia in fetal sheep. The cellular basis for this process remains unknown. We determined the impact of 2 wk of fetal hypoglycemia during late gestation on enzymes responsible for hepatic gluconeogenesis, focusing on the insulin-signaling pathway, transcription factors, and coactivators that regulate gluconeogenesis. Hepatic phosphoenolpyruvate carboxykinase and glucose-6-phosphatase mRNA increased 12-fold and 7-fold, respectively, following chronic hypoglycemia with no change in hepatic glycogen. Chronic hypoglycemia decreased fetal plasma insulin with no change in glucagon but increased plasma cortisol 3.5-fold. Peroxisome proliferator-activated receptor-gamma coactivator-1alpha mRNA and phosphorylation of cAMP response element binding protein at Ser(133) were both increased, with no change in Akt, forkhead transcription factor FoxO1, hepatocyte nuclear factor-4alpha, or CCAAT enhancer binding protein-beta. These results demonstrate that chronic fetal hypoglycemia triggers signals that can activate gluconeogenesis in the fetal liver.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0193-1849
pubmed:author
pubmed:issnType
Print
pubmed:volume
294
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E365-70
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18056789-Animals, pubmed-meshheading:18056789-Blotting, Western, pubmed-meshheading:18056789-Cloning, Molecular, pubmed-meshheading:18056789-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:18056789-Diabetes Mellitus, Type 2, pubmed-meshheading:18056789-Female, pubmed-meshheading:18056789-Fetal Growth Retardation, pubmed-meshheading:18056789-Fetus, pubmed-meshheading:18056789-Gene Expression Regulation, pubmed-meshheading:18056789-Glucose-6-Phosphatase, pubmed-meshheading:18056789-Hypoglycemia, pubmed-meshheading:18056789-Insulin, pubmed-meshheading:18056789-Liver, pubmed-meshheading:18056789-Liver Glycogen, pubmed-meshheading:18056789-Oncogene Protein v-akt, pubmed-meshheading:18056789-Phosphoenolpyruvate Carboxykinase (ATP), pubmed-meshheading:18056789-Phosphorylation, pubmed-meshheading:18056789-Pregnancy, pubmed-meshheading:18056789-RNA, Messenger, pubmed-meshheading:18056789-Receptor, Insulin, pubmed-meshheading:18056789-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18056789-Sheep, pubmed-meshheading:18056789-Transcription Factors, pubmed-meshheading:18056789-Up-Regulation
pubmed:year
2008
pubmed:articleTitle
Chronic late-gestation hypoglycemia upregulates hepatic PEPCK associated with increased PGC1alpha mRNA and phosphorylated CREB in fetal sheep.
pubmed:affiliation
Perinatal Research Center, Department of Pediatrics, University of Colorado Health Sciences Center, Aurora, CO 80045, USA. Paul.Rozance@UCHSC.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural