#Japanese name manico plus#

Specifically, we tested the hypothesis that polymorphic variation in paternally transmitted fetal IGF2 is associated with alterations in maternal glucose concentrations at week 28 of pregnancy and offspring birth weight.Ĭohorts and assessment of glucose concentrations. The current study was designed to see if the results from our mouse model ( 8), indicating that functional variation in the fetal IGF2 gene alters maternal glucose concentrations in pregnancy, could also be observed in an analogous manner in humans. This H19 single nucleotide polymorphism (SNP) was also associated with maternal glucose concentrations, suggesting that our findings in mice ( 8) may be relevant to humans. In contemporary birth cohorts, we found that in first pregnancies, cord blood IGF-II concentrations were also associated with a polymorphic variant in H19, another imprinted gene in the 11p15.5 region in humans and one that may regulate IGF2 gene expression ( 6) when transmitted from the mother to the fetus ( 13). Cord blood concentrations of its protein product, IGF-II, are associated with birth weight ( 12). In the human fetus and placenta, IGF2 is imprinted such that only the paternally transmitted copy of the gene is expressed.

The different transcripts are expressed according to their tissue and the stage of development ( 11).

#Japanese name manico plus#

Several different RNA molecules are formed upon transcription of the gene within the coding region plus one of the various 5′-untranslated regions arising from exons 1–6. The IGF2 gene comprises nine exons (codons 7–9 being coding) and four promoters, spanning a region of ∼30 kb ( 11). In humans, the IGF2 gene is located in a region rich in imprinted genes (11p15.5).

Consistent with our hypothesis, we found that intraperitoneal glucose tolerance tests indicated that mice carrying knockout offspring had increased circulating glucose concentrations in late pregnancy in comparison with those of genetically matched controls ( 8). Affected pups in this model are born ∼30% heavier than unaffected litter mates ( 9), principally as a result of biallelic Igf2 expression resulting from the disruption of its control element ( 10). We recently tested our hypothesis ( 3) in phenotypically wild type pregnant mice that were carrying pups that had a targeted 13 kb genetic region disrupted, which included the imprinted H19 gene and Igf2 control element ( 8). This is thought to be achieved through modifying fetal and placental nutritional demand and supply ( 7), potentially including altering maternal glucose concentrations ( 1, 3). Haig's kinship, or conflict hypothesis ( 5, 6), suggests that paternally expressed fetal imprinted genes will tend to increase fetal growth, whereas maternally expressed genes will tend to restrain it. Many well-characterized fetal growth genes are imprinted ( 4), meaning that they are expressed from only either the paternally or the maternally transmitted copy, depending on the gene in question and the stage of development. More recently, we suggested that in addition to the risk associated with polymorphic variation in the mother’s genes, which could affect her glucose concentrations ( 2), fetal genomic variation could also alter a mother’s risk of developing gestational diabetes mellitus (GDM) ( 3).

Almost 20 years ago it was hypothesized that polymorphic variation in the fetal genome, in particular in fetal growth genes, could lead to alterations in maternal metabolism in pregnancy ( 1).