Summary
Obesity prevalence is increasing as well as the related metabolic alterations. Obesity and T2D increase the risk of pregnancy complication and affect offspring health through developmental programming effects. Obese patients with T2D frequently present Mg2+ deficiency. During pregnancy, Mg2+ needs increases, and its insufficiency may affect the mother and fetus, interfering with pregnancy development and offspring growth. Although it is known the relevance of Mg2+, its role in pregnancy is often overlooked and the underlying mechanisms that causes disturbances on Mg2+ homeostasis are unelucidated. Mg2+ homeostasis is carefully regulated. Among the channels are the cyclin M 1-4 (CNNM1-4), highly conserved molecules. Although it has been suggested that Mg2+ transport and homeostasis plays a key role in development, its regulation during development and in maternal-fetal communication is not fully understood. Fetal growth is closely related to the placenta capacity to transport nutrients and ions. At birth, the fetus makes a transition from using placental nutrient supply to utilize the liver. Thus, changes in maternal liver metabolism related to Mg2+ levels and signalling could affect the maternal metabolic state and negatively impact the developing fetus. This project aims to assess the role of Mg2+ homeostasis and transport through the CNNMs in programming effects in the context of maternal T2D and obesity. We will focus on the role of Mg2+ on fetal programming effects in a context of altered maternal metabolism and to evaluate the impact on offspring liver. In addition, we will evaluate the potential dietary intervention with Mg2+ supplementation for ameliorating offspring-derived effects. We hypothesize that maternal obesity leads to an altered environment that involves an impaired maternal hepatic Mg2+ signaling through the CNNMs that affects the metabolic fetal environment and the maternal-fetal interaction and programs offspring metabolic alterations.
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| Web resources: | https://cordis.europa.eu/project/id/101154878 |
| Start date: | 01-09-2024 |
| End date: | 31-08-2026 |
| Total budget - Public funding: | - 181 152,00 Euro |
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Original description
Obesity prevalence is increasing as well as the related metabolic alterations. Obesity and T2D increase the risk of pregnancy complication and affect offspring health through developmental programming effects. Obese patients with T2D frequently present Mg2+ deficiency. During pregnancy, Mg2+ needs increases, and its insufficiency may affect the mother and fetus, interfering with pregnancy development and offspring growth. Although it is known the relevance of Mg2+, its role in pregnancy is often overlooked and the underlying mechanisms that causes disturbances on Mg2+ homeostasis are unelucidated. Mg2+ homeostasis is carefully regulated. Among the channels are the cyclin M 1-4 (CNNM1-4), highly conserved molecules. Although it has been suggested that Mg2+ transport and homeostasis plays a key role in development, its regulation during development and in maternal-fetal communication is not fully understood. Fetal growth is closely related to the placenta capacity to transport nutrients and ions. At birth, the fetus makes a transition from using placental nutrient supply to utilize the liver. Thus, changes in maternal liver metabolism related to Mg2+ levels and signalling could affect the maternal metabolic state and negatively impact the developing fetus. This project aims to assess the role of Mg2+ homeostasis and transport through the CNNMs in programming effects in the context of maternal T2D and obesity. We will focus on the role of Mg2+ on fetal programming effects in a context of altered maternal metabolism and to evaluate the impact on offspring liver. In addition, we will evaluate the potential dietary intervention with Mg2+ supplementation for ameliorating offspring-derived effects. We hypothesize that maternal obesity leads to an altered environment that involves an impaired maternal hepatic Mg2+ signaling through the CNNMs that affects the metabolic fetal environment and the maternal-fetal interaction and programs offspring metabolic alterations.Status
SIGNEDCall topic
HORIZON-MSCA-2023-PF-01-01Update Date
06-11-2024
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