Table 1.
The different genes whose function is linked to the development of type 2 diabetes (and its complications).
| Authors | Subjects | Tissue | Procedure | Gene | Gene function | Epigenetic change |
|---|---|---|---|---|---|---|
| Fu et al. (2004)21 | IUGR rats | Liver | Uteroplacental insufficiency | PPAR-γ Coactivator | Transcriptional coactivator, controls mRNA levels of key gluconeogenic enzymes | H3K9 hyperacetylation affecting association with gene promoter |
| Fu et al. (2004)21 | IUGR rats | Liver | Uteroplacental insufficiency | CPT-I | Part of the carnitine shuttle, rate-limiting transporter in mitochondrial fatty acid β-oxidation | H3K9 hyperacetylation affecting association with gene promoter |
| Park et al. (2008)28 | IUGR rats | Pancreatic islets | Uteroplacental insufficiency | PDX-1 | Transcription factor critical for β cell function and development | H3 and H4 deacetylation, H3K4 demethylation, H3K9 methylation |
| Raychaudhuri et al. (2008)30 | IUGR female rats | Skeletal muscle | Caloric restriction (50% of the ad libitum food intake through mid- to late pregnancy and lactation) | GLUT4 | Glucose transporter (insulin-responsive membrane-spanning glycoprotein) | H3K14 deacetylation; H3K9 methylation |
| Thompson et al. (2010)32 | IUGR rats | Pancreatic islets | Uteroplacental insufficiency | CGH-1 | Role in endothelial dysfunction (through nitric oxide synthesis) and β cell development | CpG hypermethylation in intergenic sequences |
| Thompson et al. (2010)32 | IUGR rats | Pancreatic islets | Uteroplacental insufficiency | FGFR-1 | Fibroblast Growth Factor Receptor; signaling modulated by β cell microenvironment | CpG hypomethylation in intergenic sequences |
| Thompson et al. (2010)32 | IUGR rats | Pancreatic islets | Uteroplacental insufficiency | PCSK-5 | Role in peptide processing and maturation (may impair β cell activity through IGF-I receptor- and bone morphogenetic protein 4-mediated pathways) | CpG hypermethylation in transcription start site |
| Heijmans et al. (2008)34 | Humans (AGA) | Blood | Periconceptional famine | IGF-II | Fetal growth | CpG hypomethylation |
| Barrès et al. (2009)38 | Humans (AGA) | Skeletal muscle | Incubation with TNF- α, FFA, insulin, glucose | PPAR-γ-C1-α | Transcriptional coactivator, regulator of mitochondrial genes | Non-CpG hypermethylation |
| Brøns et al. (2010)39 | Humans (SGA and AGA) | Skeletal muscle | High fat diet, overfeeding | PPAR-γ-C1-α | Transcriptional coactivator, regulator of mitochondrial genes | CpG hypermethylation |
References to the relative studies, subjects of the studies and type of epigenetic modifications are also indicated. IUGR, intrauterine growth-retarded; AGA, adequate for gestational age; SGA, small for gestational age.