Symposium: Iris's pregnancy. Function of the fetal beta cell, epigenetic and other variables
DOI:
https://doi.org/10.47196/diab.v55i3Sup.501Keywords:
prooxidant intrauterine environment, proinflammatory intrauterine environment, epigeneticAbstract
The fetal pancreas develops during the first trimester of pregnancy. The clinical history of the patient Iris shows that she was obese at the preconceptional stage, losses weight, but was still obese during the first trimester of pregnancy. Maternal obesity leads to a prooxidant and proinflammatory intrauterine environment. This may affect both the embryo beta cell differentiation process and the fine regulation needed for a proper interrelationship of the developing pancreatic islets. These are possible causes of the increased risks of metabolic dysfunction that the offspring of Iris will present during their lifetime.
The patient Iris developed gestational diabetes in the second trimester of pregnancy. Thus, in addition to the adverse effects induced by the prooxidant and proinflammatory intrauterine environment, which are increased as long as the pregnancy develops, the adverse effect of hyperglycemia arises. An excess of maternal circulating glucose will be transported to the fetal circulation through the placenta, leading to an overstimulation of the fetal pancreas, which is immature but secrete insulin. This will generate an excess of fetal insulin, and promote fetal growth, fetal adiposity and a dysregulation of the metabolic organs, which are still immature, leading to alterations that will impact the offspring in the form of metabolic programming that will be evident later in life.
The mechanisms involved in the impact of the prooxidant and proinflammatory intrauterine environment during beta cell development and pancreatic islet formation and intracellular regulations are multiple. Among them, it is relevant the epigenetic regulation and the changes in functionality of multiple transcription factors involved in the development and maturation of the endocrine pancreas. The role of nutrigenomic agents leading to the regulation of development of the endocrine pancreas to prevent fetal programming will be discussed.
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