RGD Reference Report - Proteomic Analysis of One-carbon Metabolism-related Marker in Liver of Rat Offspring. - Rat Genome Database

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Proteomic Analysis of One-carbon Metabolism-related Marker in Liver of Rat Offspring.

Authors: You, Young-Ah  Lee, Ji Hye  Kwon, Eun Jin  Yoo, Jae Young  Kwon, Woo-Sung  Pang, Myung-Geol  Kim, Young Ju 
Citation: You YA, etal., Mol Cell Proteomics. 2015 Nov;14(11):2901-9. doi: 10.1074/mcp.M114.046888. Epub 2015 Sep 4.
RGD ID: 13782135
Pubmed: PMID:26342040   (View Abstract at PubMed)
PMCID: PMC4638034   (View Article at PubMed Central)
DOI: DOI:10.1074/mcp.M114.046888   (Journal Full-text)

Maternal food intake has a significant effect on the fetal environment, and an inadequate maternal diet may result in intrauterine growth restriction. Intrauterine growth restriction newborn rat pups nursed by normal diet-fed dams exhibited rapid catch-up growth, which plays a critical role in the risk for metabolic and cardiovascular disease in later life. Specifically, one-carbon metabolism in the liver plays a critical role in placental and fetal growth. Impaired functioning of one-carbon metabolism is associated with increased homocysteine levels. In this study, we applied a comprehensive proteomic approach to identify differential expression of proteins related to one-carbon metabolism in the livers of rat offspring as an effect of maternal food restriction during gestation. Data are available via ProteomeXchange with identifier PXD002578. We determined that betaine-homocysteine S-methyltransferase 1, methylenetetrahydrofolate dehydrogenase 1, and ATP synthase subunit beta mitochondrial (ATP5B) expression levels were significantly reduced in the livers of rat offspring exposed to maternal food restriction during gestation compared with in the offspring of rats fed a normal diet (p < 0.05). Moreover, the expression levels of betaine-homocysteine S-methyltransferase 1, methylenetetrahydrofolate dehydrogenase 1, and ATP synthase subunit beta mitochondrial were negatively correlated with serum homocysteine concentration in male offspring exposed to maternal food restriction during gestation and normal diet during lactation. However, in female offspring only expression levels of methylenetetrahydrofolate dehydrogenase 1 were negatively correlated with homocysteine concentration. This study shows that maternal food restriction during late gestation and normal diet during lactation lead to increased homocysteine concentration through disturbance of one-carbon metabolism in the livers of male offspring. This suggests that male offspring have an increased gender-specific susceptibility to disease in later life through fetal programming.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
ATP5F1BHumanFetal Growth Retardation  ISOAtp5f1b (Rattus norvegicus)protein:decreased expression:liver (rat)RGD 
Atp5f1bRatFetal Growth Retardation  IEP protein:decreased expression:liver (rat)RGD 
Atp5f1bMouseFetal Growth Retardation  ISOAtp5f1b (Rattus norvegicus)protein:decreased expression:liver (rat)RGD 


Genes (Rattus norvegicus)
Atp5f1b  (ATP synthase F1 subunit beta)

Genes (Mus musculus)
Atp5f1b  (ATP synthase F1 subunit beta)

Genes (Homo sapiens)
ATP5F1B  (ATP synthase F1 subunit beta)