Hypothalamic Epac2/AKT/GnRH signalling is associated with metformin-responsive neuroendocrine improvement in a PCOS model
Na Guo, Hongyun Li, Jinhong He, Huanhuan Zhou, Xing Wang, Linlin Yang, Huijuan Ma · 2026
Read Hypothalamic Epac2/AKT/GnRH signalling is associated with metformin-responsive neuroendocrine improvement in a PCOS model by Na Guo, Hongyun Li, Jinhong He, Huanhuan Zhou, Xing Wang, Linlin Yang, Huijuan Ma (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/PMC13589382.txt.
Description
Na Guo and six colleagues trace metformin's benefit in polycystic ovary syndrome up into the brain's hormone control center. The syndrome involves overactive release of gonadotropin-releasing hormone, and metformin helps many patients, but its brain-side action was murky. Working in 2026, the team treated rats with a drug-induced version of the syndrome, profiled hypothalamus proteins, and probed a hormone-producing cell line made insulin resistant.
Metformin eased the rats' insulin resistance, hormone overshoot, broken cycles, and ovary changes. Protein maps pointed at insulin and cAMP signaling, and in the cells, metformin restored a protein called Epac2 and its downstream AKT signal while calming hormone overproduction. Silencing Epac2 in the mouse hypothalamus reproduced insulin resistance and hormone excess. The authors conclude the Epac2 pathway helps carry metformin's central benefit, with more work needed on the balance between brain and body effects.
Catalog record
| CREATOR | Na Guo, Hongyun Li, Jinhong He, Huanhuan Zhou, Xing Wang, Linlin Yang, Huijuan Ma |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 67 KB |
| LICENSE | https://creativecommons.org/licenses/by/4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |