Document Detail


Developmental changes in the expression of creatine synthesizing enzymes and creatine transporter in a precocial rodent, the spiny mouse.
MedLine Citation:
PMID:  19570237     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Creatine synthesis takes place predominately in the kidney and liver via a two-step process involving AGAT (L-arginine:glycine amidinotransferase) and GAMT (guanidinoacetate methyltransferase). Creatine is taken into cells via the creatine transporter (CrT), where it plays an essential role in energy homeostasis, particularly for tissues with high and fluctuating energy demands. Very little is known of the fetal requirement for creatine and how this may change with advancing pregnancy and into the early neonatal period. Using the spiny mouse as a model of human perinatal development, the purpose of the present study was to comprehensively examine the development of the creatine synthesis and transport systems.
RESULTS: The estimated amount of total creatine in the placenta and brain significantly increased in the second half of pregnancy, coinciding with a significant increase in expression of CrT mRNA. In the fetal brain, mRNA expression of AGAT increased steadily across the second half of pregnancy, although GAMT mRNA expression was relatively low until 34 days gestation (term is 38-39 days). In the fetal kidney and liver, AGAT and GAMT mRNA and protein expression were also relatively low until 34-37 days gestation. Between mid-gestation and term, neither AGAT or GAMT mRNA or protein could be detected in the placenta.
CONCLUSION: Our results suggest that in the spiny mouse, a species where, like the human, considerable organogenesis occurs before birth, there appears to be a limited capacity for endogenous creatine synthesis until approximately 0.9 of pregnancy. This implies that a maternal source of creatine, transferred across the placenta, may be essential until the creatine synthesis and transport system matures in preparation for birth. If these results also apply to the human, premature birth may increase the risk of creatine deficiency.
Authors:
Zoe Ireland; Aaron P Russell; Theo Wallimann; David W Walker; Rod Snow
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-07-01
Journal Detail:
Title:  BMC developmental biology     Volume:  9     ISSN:  1471-213X     ISO Abbreviation:  BMC Dev. Biol.     Publication Date:  2009  
Date Detail:
Created Date:  2009-07-21     Completed Date:  2009-09-25     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  100966973     Medline TA:  BMC Dev Biol     Country:  England    
Other Details:
Languages:  eng     Pagination:  39     Citation Subset:  IM    
Affiliation:
Department of Physiology, Monash University, Clayton, Australia 3800. zoe.ireland@med.monash.edu.au
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MeSH Terms
Descriptor/Qualifier:
Amidinotransferases / genetics*
Animals
Animals, Newborn
Brain / enzymology,  metabolism
Creatine / metabolism*
Female
Fetus / enzymology,  metabolism
Gene Expression Regulation, Developmental*
Guanidinoacetate N-Methyltransferase / genetics*
Immunoblotting
Kidney / enzymology
Liver / enzymology
Membrane Transport Proteins / genetics*
Mice
Placenta / enzymology,  metabolism
Polymerase Chain Reaction
Pregnancy
RNA, Messenger / genetics
Chemical
Reg. No./Substance:
0/Membrane Transport Proteins; 0/RNA, Messenger; 0/creatine transporter; 57-00-1/Creatine; EC 2.1.1.2/Guanidinoacetate N-Methyltransferase; EC 2.1.4.-/Amidinotransferases; EC 2.1.4.1/glycine amidinotransferase
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