Publicaciones académicas

@article{nokey,

title = {Developmental programming of the offspring´s health and disease by maternal obesity},

author = {María Luisa Garmendia },

doi = {10.1016/j.placenta.2024.05.006},

year  = {2024},

date = {2024-08-05},

journal = {Placenta},

abstract = {- Otros autores: Lépez M, Bellalta S, Carrasco-Negüe K, Castaño-Moreno E, Jaramillo-Ospina A, Araujo K, Etchegaray K, Navarro C, Gómez-Cayupán J, Valenzuela R, Casanello P.



- Cómo citar: Macarena Lépez, Sofía Bellalta, Karina Carrasco-Negüe, Erika Castaño-Moreno, Ángela Jaramillo-Ospina, Kenny Araujo, Karina Etchegaray, Carmen Navarro, Jorge Gómez-Cayupán, Rodrigo Valenzuela, María Luisa Garmendia, Paola Casanello,

Developmental programming of the offspring´s health and disease by maternal obesity, Placenta, Volume 153, 2024, Page e3,

ISSN 0143-4004, https://doi.org/10.1016/j.placenta.2024.05.006.



- Resumen: Maternal obesity is the most relevant risk factor for developing childhood obesity and metabolic syndrome in the offspring. The mother’s inflammatory and metabolic status can be transferred to the developing embryo and fetus, which can program cell metabolism. In this presentation, a short review of the mechanisms by which maternal obesity can alter the fetal immune function, fetal adiposity, and placental function will be described. We set the study at birth and follow-up (4 months) of the offspring of women with pregestational obesity who participated in a randomized controlled trial of docosahexaenoic acid (DHA) supplementation during pregnancy. The results of this follow-up on neonatal body composition, immune function, and methylome, metabolic markers (lipid profile, HOMA-IR, leptin, adiponectin), and placental markers of inflammation and fatty acid transporters will be presented and discussed. The results presented will shed light on our current research interest, where the mechanism by which the inflammatory intrauterine environment could alter the offspring´s progenitor hematopoietic and mesenchymal stem cells, compromising their early cell commitment. These molecular changes are critical to the infant´s programming of the risk of obesity and chronic diseases and are fundamental to understanding how and when prevention needs to start.},

keywords = {L4: Ventanas Críticas del Desarrollo: Materno-Infantil.   /},

pubstate = {published},

tppubtype = {article}

}

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- Otros autores: Lépez M, Bellalta S, Carrasco-Negüe K, Castaño-Moreno E, Jaramillo-Ospina A, Araujo K, Etchegaray K, Navarro C, Gómez-Cayupán J, Valenzuela R, Casanello P.

- Cómo citar: Macarena Lépez, Sofía Bellalta, Karina Carrasco-Negüe, Erika Castaño-Moreno, Ángela Jaramillo-Ospina, Kenny Araujo, Karina Etchegaray, Carmen Navarro, Jorge Gómez-Cayupán, Rodrigo Valenzuela, María Luisa Garmendia, Paola Casanello,
Developmental programming of the offspring´s health and disease by maternal obesity, Placenta, Volume 153, 2024, Page e3,
ISSN 0143-4004, https://doi.org/10.1016/j.placenta.2024.05.006.

- Resumen: Maternal obesity is the most relevant risk factor for developing childhood obesity and metabolic syndrome in the offspring. The mother’s inflammatory and metabolic status can be transferred to the developing embryo and fetus, which can program cell metabolism. In this presentation, a short review of the mechanisms by which maternal obesity can alter the fetal immune function, fetal adiposity, and placental function will be described. We set the study at birth and follow-up (4 months) of the offspring of women with pregestational obesity who participated in a randomized controlled trial of docosahexaenoic acid (DHA) supplementation during pregnancy. The results of this follow-up on neonatal body composition, immune function, and methylome, metabolic markers (lipid profile, HOMA-IR, leptin, adiponectin), and placental markers of inflammation and fatty acid transporters will be presented and discussed. The results presented will shed light on our current research interest, where the mechanism by which the inflammatory intrauterine environment could alter the offspring´s progenitor hematopoietic and mesenchymal stem cells, compromising their early cell commitment. These molecular changes are critical to the infant´s programming of the risk of obesity and chronic diseases and are fundamental to understanding how and when prevention needs to start.

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