Fetal manipulation of maternal metabolism is a critical function of the imprinted Igf2 gene.
Cell Metab
; 35(7): 1195-1208.e6, 2023 07 11.
Article
en En
| MEDLINE
| ID: mdl-37437545
ABSTRACT
Maternal-offspring interactions in mammals involve both cooperation and conflict. The fetus has evolved ways to manipulate maternal physiology to enhance placental nutrient transfer, but the mechanisms involved remain unclear. The imprinted Igf2 gene is highly expressed in murine placental endocrine cells. Here, we show that Igf2 deletion in these cells impairs placental endocrine signaling to the mother, without affecting placental morphology. Igf2 controls placental hormone production, including prolactins, and is crucial to establish pregnancy-related insulin resistance and to partition nutrients to the fetus. Consequently, fetuses lacking placental endocrine Igf2 are growth restricted and hypoglycemic. Mechanistically, Igf2 controls protein synthesis and cellular energy homeostasis, actions dependent on the placental endocrine cell type. Igf2 loss also has additional long-lasting effects on offspring metabolism in adulthood. Our study provides compelling evidence for an intrinsic fetal manipulation system operating in placenta that modifies maternal metabolism and fetal resource allocation, with long-term consequences for offspring metabolic health.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Placenta
/
Resistencia a la Insulina
/
Factor II del Crecimiento Similar a la Insulina
Límite:
Animals
/
Pregnancy
Idioma:
En
Revista:
Cell Metab
Asunto de la revista:
METABOLISMO
Año:
2023
Tipo del documento:
Article