Authors
Jianning Liao, Qinghua Liu, Cong Liu, Guiqiong Liu, Xiang Li, Xiaodong Wang, Yaqin Wang, Ruiyan Liu, Hao Wu, Chaoli Wang, Hongru Shi, Yongheng Zhao, Wenkai Ke, Zaohong Ran, Zian Wu, Bowen Tan, Quanfeng Wang, Guohua Hua, Shujun Zhang, Qingzhen Xie, Guoshi Liu, Changjiu He
Published in
Proceedings of the National Academy of Sciences of the United States of America. Volume 123. Issue 27. Pages e2523789123. Jul 07, 2026. Epub Jul 01, 2026.
Abstract
The corpus luteum (CL) arises from the luteinization of granulosa cells (GCs) and theca cells, marked by rapid progesterone elevation and angiogenesis. Intriguingly, angiogenesis lags behind progesterone elevation, creating an avascular phase during which luteal cells must fuel intensive steroidogenesis without perfusion. How the avascular CL meets this energetic demand remains a mystery. Here, we reveal a cellular adaptive mechanism-granulosa cell energy storage (GCES)-that resolves this enigma. We demonstrate that upon luteinization initiation, GCs enter a metabolically quiescent state yet enhance glucose uptake, converting the glucose into glycogen. Catabolism of this glycogen reserve supplies the energy required for the avascular CL, ensuring normal luteogenesis. Disruption of GCES induces luteal insufficiency, whereas timely glucose administration enhances GCES, improving luteal function and optimizing reproductive outcome in both mouse and ovine models. In human study, oral intake of glucose post-hCG significantly augments GCES and enhances progesterone production. These results advance our understanding of luteinization.
PMID:
42384696
Bibliographic data and abstract were imported from PubMed on 02 Jul 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 13
- Comments 0