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Embryonic diapause (ED) is a temporary arrest of an embryo when it waits for the uterine receptivity signal to implant. We provide evidence that LDs play a crucial role in maintaining ED. Diapausing embryos exhibit increased release of exosomes reflecting elevated embryonic signaling to the mother. During ED, the decrease in lipid is caused by a switch from carbohydrate metabolism to lipid catabolism. We have also shown that presence of LDs in the oocytes of various mammals positively corelates with their species-specific length of diapause. 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