Epigenetic deregulation of imprinting in congenital diseases of aberrant growth

Delaval, Katia; Wagschal, Alexandre; Feil, Robert

doi:10.1002/bies.20407

Cited by 103 publications

(64 citation statements)

References 64 publications

(93 reference statements)

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“…There are also a number of well-documented examples from natural history that show variation in the phenotype of the offspring in response to changes in the maternal environment during pregnancy. [3][4][5] It is, therefore, unsurprising that the quality of the developmental environment to which humans embryos are exposed is able to induce lifelong changes in the phenotype of the children both in terms of morphology 6,7 and metabolism. Gross morphological variation in response to the early-life environment is relatively rare.…”

Section: The Developmental Origins Of Human Metabolic Diseasementioning

confidence: 99%

Epigenetic changes in early life and future risk of obesity

2010

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The rapid increase in incidence of obesity over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environments also strongly influence the risk of developing obesity in later life. Initially, human studies showed that low birth weight was associated with an increased risk of obesity but increasingly there is evidence that overnutrition in the early life can also increase susceptibility to future obesity. These findings have now been replicated in animal models, which have shown that both maternal under-and overnutrition can induce persistent changes in gene expression and metabolism. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. In this review, we discuss the recent evidence that shows that early-life environment can induce altered epigenetic regulation leading to the induction of an altered phenotype. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of obesity opens the possibility that interventions, either through nutrition or specific drugs, may modify long-term obesity risk and combat this rapid rise in obesity.

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Section: The Developmental Origins Of Human Metabolic Diseasementioning

confidence: 99%

Epigenetic changes in early life and future risk of obesity

2010

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“…[6][7][8] In humans, low IGF2 expression levels due to epigenetic modifications have been observed in patients with the Silver-Russell syndrome, which is characterized by severe intrauterine and postnatal growth retardation. 9,10 Conversely, overexpression of IGF2 due to different reasons is frequently observed in patients with the Beckwith-Wiedemann syndrome, which is a fetal overgrowth disorder. 10,11 Although IGF2 is transcribed at a lower level after birth, several studies suggest that IGF2 may also have metabolic effects postnatally.…”

Section: Introductionmentioning

confidence: 99%

“…9,10 Conversely, overexpression of IGF2 due to different reasons is frequently observed in patients with the Beckwith-Wiedemann syndrome, which is a fetal overgrowth disorder. 10,11 Although IGF2 is transcribed at a lower level after birth, several studies suggest that IGF2 may also have metabolic effects postnatally. For instance, transgenic mice overexpressing Igf2 in the adult liver were found to have an increased insulin-stimulated glucose uptake and a lower fat body mass.…”

Section: Introductionmentioning

confidence: 99%

Parent-of-origin specific linkage and association of the IGF2 gene region with birth weight and adult metabolic risk factors

et al. 2009

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Objective: The maternally imprinted insulin-like growth factor 2 (IGF2) gene is an important fetal growth factor and is also suggested to have postnatal metabolic effects. In this study, we examined whether common polymorphisms in IGF2 (6815_6819delAGGGC, 1156T4C and 820G4A (ApaI)) and a microsatellite marker in the close vicinity of IGF2 were linked to or associated with birth weight and adult metabolic risk factors. Design and participants: Polymorphisms were genotyped in 199 monozygotic complete twin pairs, 109 dizygotic complete twin pairs, 15 single twins, 231 mothers and 228 fathers recruited from the East Flanders Prospective Twin Survey. Conventional and parent-of-origin specific linkage and association analyses were carried out with birth weight, adult body height and parameters quantifying obesity, insulin sensitivity and dyslipidaemia measured at adult age (mean age 25 years). Results: In the parent-of-origin specific association analysis, in which only the paternally inherited allele was incorporated, the 1156T4C SNP (single nucleotide polymorphism) showed significant association with IGF-binding protein 1 (IGFBP1) levels (T and C (mean (95% CI)): 13.2 (12.1-14.3) and 16.2 (14.6-18.0) ng ml À1 , P ¼ 0.002). No linkage was observed in either the conventional or in the parent-of-origin specific linkage analysis. Conclusion: This study suggests that paternally inherited alleles of a common polymorphism in the IGF2 gene affect IGFBP1 levels.

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“…Oppositely, the overexpression of IGF2 in humans causes the Beckwith-Wiedemann syndrome (BWS), characterized by biallelic methylation of IGF2-H19 ICR, lack of H19 expression, and biallelic expression of IGF2. The individual affected by BWS shows pre-and postnatal overgrowth, organomegaly and neonatal hypoglycemia (Delaval et al, 2006). Similarly, the overexpression of Igf2 in mice promotes fetal overgrowth (Eggenschwiler et al, 1997), while underexpression of Igf2 was associated with a deficit in growth (DeChiara et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Imprinted gene expression in in vivo- and in vitro-produced bovine embryos and chorio-allantoic membranes

Perecin

Méo²,

Yamazaki³

et al. 2009

Genet. Mol. Res.

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AbStRACt. Cloning by nuclear transfer is often associated with poor results due to abnormal nuclear reprogramming of somatic donor cells and altered gene expression patterns. We investigated the expression patterns of imprinted genes IGF2 and IGF2R in 33-to 36-day bovine embryos and chorio-allantoic membranes derived from in vivo-and in vitro-produced embryos by somatic cell nuclear transfer (SCNT), parthenogenetic activation, and in vitro fertilization (IVF). There was a lower IGF2 expression rate in the SCNT (0.19) and parthenogenetic (0.02) groups when compared to in vivo and IVF embryos (2.01; P < 0.05). In the chorio-allantoic membranes, IGF2 showed a baseline expression pattern (P < 0.05) in parthenotes (0.001) when compared to in vivo, IVF (3.13), and SCNT (0.98) groups. IGF2R was less expressed (P < 0.05) in SCNT chorio-allantoic membranes (0.25) when compared to the in vivo group. The low expression of IGF2 in parthenogenetic embryos and Alterations in the relative frequency of IGF2 and IGF2R transcripts were observed in SCNT-derived bovine embryos and chorioallantoic membranes, respectively, supporting the hypothesis that abnormalities in the expression of imprinted genes are causes of the low efficiency of SCNT procedures in this species.

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Epigenetic deregulation of imprinting in congenital diseases of aberrant growth

Cited by 103 publications

References 64 publications

Epigenetic changes in early life and future risk of obesity

Epigenetic changes in early life and future risk of obesity

Parent-of-origin specific linkage and association of the IGF2 gene region with birth weight and adult metabolic risk factors

Imprinted gene expression in in vivo- and in vitro-produced bovine embryos and chorio-allantoic membranes

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