PMID- 15259033
OWN - NLM
STAT- MEDLINE
DCOM- 20050201
LR  - 20131121
IS  - 1542-0752 (Print)
IS  - 1542-0752 (Linking)
VI  - 70
IP  - 7
DP  - 2004 Jul
TI  - In vivo hyperglycemia and its effect on Glut-1 expression in the embryonic heart.
PG  - 438-48
AB  - BACKGROUND: Maternal diabetes exposes embryos to periods of hyperglycemia. 
      Glucose is important for normal cardiogenesis, and Glut-1 is the predominant 
      glucose transporter in the embryo. METHODS: Pregnant mice were exposed to 6 or 12 
      hr hyperglycemia during organogenesis using intraperitoneal (IP) injections of 
      D-glucose on gestational day (GD) 9.5 (plug = GD 0.5). Embryos were examined for 
      morphology and total cardiac protein, and embryonic hearts were evaluated for 
      Glut-1 protein and mRNA expression immediately after treatment (GD 9.75, GD 
      10.0), as well as on GD 10.5 and GD 12.5. RESULTS: IP glucose injections were 
      effective in producing sustained maternal hyperglycemia. Maternal hyperglycemia 
      for 6 or 12 hr on GD 9.5, followed by normoglycemia, produced a decrease in 
      overall size and total cardiac protein in embryos evaluated on GD 10.5 but no 
      difference on GD 12.5. Cardiac Glut-1 expression was immediately upregulated in 
      embryos exposed to 6 or 12 hr maternal hyperglycemia. On GD 10.5, cardiac Glut-1 
      expression was not different in embryos exposed to maternal hyperglycemia for 6 
      hr but was downregulated in embryos exposed for 12 hr. On GD 12.5, cardiac Glut-1 
      expression in embryos exposed to maternal hyperglycemia on GD 9.5 for 6 or 12 hr, 
      followed by normoglycemia, was not different from controls. The temporal pattern 
      was the same for Glut-1 protein and mRNA expression. CONCLUSIONS: 
      Hyperglycemia-induced alterations in Glut-1 expression likely interfere with 
      balance of glucose available to the embryonic heart that may affect cardiac 
      morphogenesis.
FAU - Joyner, Nia T
AU  - Joyner NT
AD  - Department of Molecular Biomedical Sciences, College of Veterinary Medicine, 
      North Carolina State University, Raleigh, North Carolina, USA. 
      ntjoyner@unity.ncsu.edu
FAU - Smoak, Ida W
AU  - Smoak IW
LA  - eng
GR  - HL-60752/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Birth Defects Res A Clin Mol Teratol
JT  - Birth defects research. Part A, Clinical and molecular teratology
JID - 101155107
RN  - 0 (Glucose Transporter Type 1)
RN  - 0 (Monosaccharide Transport Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Slc2a1 protein, mouse)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Female
MH  - Gene Expression/physiology
MH  - Glucose/*metabolism
MH  - Glucose Transporter Type 1
MH  - Heart/*embryology
MH  - Hyperglycemia/*metabolism
MH  - Mice
MH  - Monosaccharide Transport Proteins/genetics/*metabolism
MH  - Pregnancy
MH  - RNA, Messenger/metabolism
EDAT- 2004/07/20 05:00
MHDA- 2005/02/03 09:00
CRDT- 2004/07/20 05:00
PHST- 2004/07/20 05:00 [pubmed]
PHST- 2005/02/03 09:00 [medline]
PHST- 2004/07/20 05:00 [entrez]
AID - 10.1002/bdra.20046 [doi]
PST - ppublish
SO  - Birth Defects Res A Clin Mol Teratol. 2004 Jul;70(7):438-48. doi: 
      10.1002/bdra.20046.