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Updated: Aug 6, 2026

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Establishment of an Embryo Implantation Model In Vitro
Published on: June 21, 2024
Ghrelin impairs embryo development after ovarian hyperstimulation
Ramírez Nicolás David1,2, Schulman Fernández Martín1, Torres Pedro Javier1
1Instituto de Fisiología, Cátedra de Fisiología Humana, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba , Córdoba, Argentina.
The Journal of Endocrinology
|July 16, 2026
Summary
Controlled ovarian hyperstimulation (COH) increases ghrelin, negatively impacting embryo development. Blocking the ghrelin receptor reversed these effects, suggesting a new therapeutic target for assisted reproduction.
Area of Science:
- Reproductive Biology
- Endocrinology
- Developmental Biology
Background:
- Controlled ovarian hyperstimulation (COH) is crucial for assisted reproductive technologies.
- COH has been linked to reduced reproductive success.
- COH elevates circulating ghrelin, but its role in COH-induced effects is unclear.
Purpose of the Study:
- To investigate the impact of COH on preimplantation embryo development and implantation in a murine model.
- To determine if COH-induced alterations are associated with hyperghrelinemia.
- To evaluate the therapeutic potential of ghrelin receptor antagonists.
Main Methods:
- Evaluated hormonal profiles, oocyte and embryo quality, implantation rates, and decidual characteristics in mice.
- Compared mice in natural cycles (controls) with those undergoing COH.
- Administered ghrelin receptor antagonists ((D-Lys3)-GHRP-6 or PF-5190457) to COH-treated mice.
Main Results:
- COH increased ovulation, progesterone, and ghrelin levels but did not affect oocyte quality.
- COH delayed embryo development, which was reversed by ghrelin receptor antagonists.
- COH reduced uterine IL-6 expression, restored by ghrelin blockade, suggesting an immune-mediated mechanism.
Conclusions:
- COH-induced hyperghrelinemia negatively impacts embryo development.
- Ghrelin receptor blockade can reverse COH-induced delays in embryo development.
- COH may alter the uterine immune microenvironment, affecting reproductive outcomes.
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