DNA methylation changes in genes coding for leptin and insulin receptors during metabolic-altered pregnancies
| Autor: | Patricia Ojeda-Provoste, Luis Sobrevia, Sharin Valdivia, Bredford Kerr, Fernando Toledo, Francisca Stolzenbach |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Leptin Placenta 030209 endocrinology & metabolism Biology Bioinformatics Epigenesis Genetic Fetal Development 03 medical and health sciences 0302 clinical medicine Metabolic Diseases Pregnancy medicine Homeostasis Humans Insulin Epigenetics Obesity Receptor Molecular Biology reproductive and urinary physiology Fetus Leptin receptor DNA Methylation Receptor Insulin Insulin receptor 030104 developmental biology medicine.anatomical_structure embryonic structures DNA methylation biology.protein Molecular Medicine Receptors Leptin Female Signal Transduction |
| Zdroj: | Biochimica et biophysica acta. Molecular basis of disease. 1866(2) |
| ISSN: | 1879-260X |
| Popis: | The overwhelming rates of obesity worldwide are a major concern due to the elevated medical costs associated and the poor quality of life of obese patients. In the recent years, it has become evident that the intrauterine milieu can have a long-term impact on the foetus health. The placenta is a highly dynamic organ; whose primary function is to carry nutrients from the mother to the foetus and to remove waste products from the foetus. Any alteration in maternal circulating metabolites elicits a response in order to ensure the developing foetus an adequate growth environment. This response can be translated into epigenetic modifications in coding genes for metabolic-related receptors located in the placenta and foetal tissues. The most studied receptors involved in the metabolic sensing are the leptin and the insulin receptors. A maternal metabolic disease-like state can alter the expression of these receptors in different organs, including placenta. There is evidence that these alterations not only affect the expression level of these receptors, but there are also differences in epigenetic marks in regulatory elements of these genes that may become permanent despite the mother's treatment. This review provides evidence about possible mechanisms involved in the foetal programming of metabolic diseases originated from the pre-natal environment that could contributive to increasing levels of obesity in the world. |
| Databáze: | OpenAIRE |
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