Histone Code Modifications Repress Glucose Transporter 4 Expression in the Intrauterine Growth-restricted Offspring

Raychaudhuri, Nupur; Raychaudhuri, Santanu; Thamotharan, Manikkavasagar; Devaskar, Sherin U.

doi:10.1074/jbc.m800128200

Cited by 206 publications

(160 citation statements)

References 66 publications

(95 reference statements)

Supporting

Mentioning

156

Contrasting

Unclassified

Order By: Relevance

“…7 There is evidence showing that early exposure to suboptimal environment induces epigenetic changes predisposing to type 2 diabetes (Table 1). [22][23][24][25] In rats, the exposure to uteroplacental insufficiency induces hepatic DNA hypomethylation and histone hyperacetylation of histone H3 on lysine 9 (H3K9), lysine 14 (H3K14) and lysine 18 (H3K18) at birth 26 These changes persist up to day 21 of postnatal life, suggesting a permanent effect on hepatic gene expression. The hyperacetylation on histone H3 in the liver of IUGR rats occurs in association with decreased nuclear protein levels of histone deacetylase 1 (HDAC1) and HDAC activity.…”

Section: The Mechanisms Of Programmingmentioning

confidence: 99%

“…34 Interestingly, the subjects exposed to famine periconceptionally showed, 60 years later, decreased methylation of IGF-II, whereas no change in the degree of IGF-II methylation was observed in those exposed to famine late in gestation. 35 The reduced methylation of IGF-II may represent the 22 Liver CPT-I Rate-limiting transporter in mitochondrial fatty acid b-oxidation H3K9 hyperacetylation affecting association with gene promoter IUGR rats 23 Pancreatic islets PDX-1 Transcription factor critical for b-cell function and development H3 and H4 deacetylation, H3K4 demethylation, H3K9 methylation IUGR rats 24 Skeletal muscle GLUT4 Glucose transporter H3K14 de-acetylation; H3K9 methylation IUGR rats 25 Pancreatic islets CGH-1 Role in endothelial dysfunction and b-cell development CpG hypermethylation in intergenic sequences IUGR rats 25 Pancreatic islets FGFR-1 Fibroblast growth factor receptor CpG hypomethylation in intergenic sequences IUGR rats 25 Pancreatic islets PCSK-5 Role in peptide processing and maturation CpG hypermethylation in transcription start site Humans 35 Blood IGF-II Fetal growth CpG hypomethylation…”

Section: Evidence For Programmingmentioning

confidence: 99%

See 1 more Smart Citation

Effect of intrauterine growth retardation on liver and long-term metabolic risk

Cianfarani

Agostoni

Bedogni³

et al. 2012

Int J Obes

View full text Add to dashboard Cite

Intrauterine growth retardation predisposes toward long-term morbidity from type 2 diabetes and cardiovascular disease. To explain this association, the concept of programming was introduced to indicate a process whereby a stimulus or insult at a critical period of development has lasting or lifelong consequences on key endocrine and metabolic pathways. Subtle changes in cell composition of tissues, induced by suboptimal conditions in utero, can influence postnatal physiological functions. There is increasing evidence, suggesting that liver may represent one of the candidate organs targeted by programming, undergoing structural, functional and epigenetic changes following exposure to an unfavorable intrauterine environment. The aim of this review is to provide insights into the molecular mechanisms underlying liver programming that contribute to increase the cardiometabolic risk in subjects with intrauterine growth restriction.

show abstract

Section: The Mechanisms Of Programmingmentioning

confidence: 99%

Section: Evidence For Programmingmentioning

confidence: 99%

Effect of intrauterine growth retardation on liver and long-term metabolic risk

Cianfarani

Agostoni

Bedogni³

et al. 2012

Int J Obes

View full text Add to dashboard Cite

show abstract

“…Progression of these histone modifications parallels the progressive decrease in Pdx-1 expression which locks in the silenced state in the IUGR adult pancreas resulting in diabetes (43) . Similarly, Raychaudhuri et al (44) demonstrated that perinatal nutrient restriction resulting in IUGR leads to histone modifications in skeletal muscle that directly decrease GLUT type 4 (Glut4) gene expression. This effectively creates a metabolic knockdown of this important regulator of peripheral glucose transport and insulin resistance, thereby contributing to adult type 2 diabetes (44) .…”

Section: Epigenetic Mechanisms Elicited By Maternal Diet During Pregnmentioning

confidence: 99%

Epigenetic mechanisms elicited by nutrition in early life

et al. 2011

View full text Add to dashboard Cite

A growing number of studies focusing on the developmental origin of health and disease hypothesis have identified links among early nutrition, epigenetic processes and diseases also in later life. Different epigenetic mechanisms are elicited by dietary factors in early critical developmental ages that are able to affect the susceptibility to several diseases in adulthood. The studies here reviewed suggest that maternal and neonatal diet may have long-lasting effects in the development of non-communicable chronic adulthood diseases, in particular the components of the so-called metabolic syndrome, such as insulin resistance, type 2 diabetes, obesity, dyslipidaemia, hypertension, and CVD. Both maternal under-and over-nutrition may regulate the expression of genes involved in lipid and carbohydrate metabolism. Early postnatal nutrition may also represent a vital determinant of adult health by making an impact on the development and function of gut microbiota. An inadequate gut microbiota composition and function in early life seems to account for the deviant programming of later immunity and overall health status. In this regard probiotics, which have the potential to restore the intestinal microbiota balance, may be effective in preventing the development of chronic immune-mediated diseases. More recently, the epigenetic mechanisms elicited by probiotics through the production of SCFA are hypothesised to be the key to understand how they mediate their numerous health-promoting effects from the gut to the peripheral tissues.

show abstract

“…A number of studies suggest that uteroplacental insufficiency, a common cause of IUGR, induces epigenetic modifications in offspring (97)(98)(99)(100) . Epigenetic modifications affecting processes important to glucose regulation and insulin secretion, characteristics essential to the pathophysiology of T2D have been described in the IUGR liver, pancreatic b-cells and muscle (97)(98)(99)(100) .…”

Section: Epigenetic Regulation Of Gene Expression In Fetal Growth Retmentioning

confidence: 99%

“…Epigenetic modifications affecting processes important to glucose regulation and insulin secretion, characteristics essential to the pathophysiology of T2D have been described in the IUGR liver, pancreatic b-cells and muscle (97)(98)(99)(100) .…”

Section: Epigenetic Regulation Of Gene Expression In Fetal Growth Retmentioning

confidence: 99%

Epigenetics and maternal nutrition: nature v. nurture

Simmons

2010

Proc. Nutr. Soc.

View full text Add to dashboard Cite

Under- and over-nutrition during pregnancy has been linked to the later development of diseases such as diabetes and obesity. Epigenetic modifications may be one mechanism by which exposure to an altered intrauterine milieu or metabolic perturbation may influence the phenotype of the organism much later in life. Epigenetic modifications of the genome provide a mechanism that allows the stable propagation of gene expression from one generation of cells to the next. This review highlights our current knowledge of epigenetic gene regulation and the evidence that chromatin remodelling and histone modifications play key roles in adipogenesis and the development of obesity. Epigenetic modifications affecting processes important to glucose regulation and insulin secretion have been described in the pancreatic β-cells and muscle of the intrauterine growth-retarded offspring, characteristics essential to the pathophysiology of type-2 diabetes. Epigenetic regulation of gene expression contributes to both adipocyte determination and differentiation in in vitro models. The contributions of histone acetylation, histone methylation and DNA methylation to the process of adipogenesis in vivo remain to be evaluated.

show abstract

Histone Code Modifications Repress Glucose Transporter 4 Expression in the Intrauterine Growth-restricted Offspring

Abstract: We examined transcriptional and epigenetic mechanism(s) behind diminished skeletal muscle GLUT4 mRNA in intrauterine growth-restricted (IUGR) female rat offspring. An increase in MEF2D (inhibitor) with a decline in MEF2A (

Cited by 206 publications

References 66 publications

Effect of intrauterine growth retardation on liver and long-term metabolic risk

Effect of intrauterine growth retardation on liver and long-term metabolic risk

Epigenetic mechanisms elicited by nutrition in early life

Epigenetics and maternal nutrition: nature v. nurture

Contact Info

Product

Resources

About