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In vitro fertilization causes excessive glycogen accumulation in mouse placenta
Jie Dong1, Xiangyu Guo2, Chenxi Qian1
1Department of Obstetrics and Gynaecology, Tangdu Hospital, Air Force Medical University, Xi'an, 710038, Shaanxi, China.
Placenta
|August 21, 2021
Summary
Assisted reproductive technologies like in vitro fertilization (IVF) enlarge placentas and increase glycogen storage in mice. This may be linked to the Akt-Gsk3β pathway, impacting fetal development.
Area of Science:
- Reproductive biology
- Developmental biology
- Metabolic research
Background:
- Assisted reproductive technologies (ART) are linked to adverse pregnancy outcomes.
- Placental function, particularly glycogen metabolism, is crucial for fetal growth and health.
- Mechanisms underlying ART-related placental complications remain unclear.
Purpose of the Study:
- To investigate the impact of in vitro fertilization (IVF) on placental glycogen storage in a mouse model.
- To explore the role of glycogen metabolism and the Akt-Gsk3β pathway in IVF-associated placental changes.
Main Methods:
- Collected mouse placentas at E18.5 following natural mating or IVF.
- Measured placental and fetal weights.
- Quantified glycogen content and analyzed gene expression related to glycogen metabolism, glucose transport, and Akt/Gsk3β phosphorylation.
Main Results:
- IVF resulted in significantly increased placental weight and junctional area.
- Excessive glycogen accumulation was observed in IVF placentas.
- Decreased mRNA levels of genes involved in glycogen synthesis andolysis, and reduced expression of key enzymes and glucose transporters were noted.
- Inhibition of Akt and Gsk3β phosphorylation was detected in IVF placentas.
Conclusions:
- IVF induces placental enlargement and abnormal glycogen storage in late pregnancy in mice.
- These alterations are potentially mediated by the Akt-Gsk3β signaling pathway.
- Further research is needed to understand the long-term implications for offspring health.

