ArticleReproduction (Cambridge, England)2025
The kisspeptin analog C6 reverses reproductive dysfunction in a mouse model of hyperprolactinemia.
Article in Reproduction (Cambridge, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In brief: Kisspeptin has been shown to be tightly associated with hyperprolactinemia. This study shows that similar to kisspeptin, its analog C6 produces a reversal of HPRL estrus cycle and ovulation disruption. Abstract: HPRL, characterized by elevated prolactin levels, disrupts the hypothalamic-pituitary-gonadal axis, leading to reproductive dysfunctions such as menstrual irregularities, anovulation and infertility. Current treatments rely on dopamine agonists but are limited by side effects and resistance. Kisspeptin (Kp), a key neuropeptide regulating the reproductive function, offers potential as an alternative therapy. However, Kp's short half-life requires impractical administration regimens. To address this, we developed a synthetic Kp analog, C6, with enhanced pharmacokinetics. This study evaluated the effects of C6 compared to Kp in a mouse model of HPRL. Mice received subcutaneous PRL injections for 21 days to induce HPRL, followed by daily or alternate-day intraperitoneal administration of Kp10, C6 or vehicle. Estrous cyclicity, luteinizing hormone (LH) secretion, ovarian histology and hypothalamic gene expression were analyzed. As expected, the HPRL treatment blocked estrous activity, which was restored by both Kp10, the shortest bioactive isoform of Kp, and C6. Histological analysis revealed increased corpora lutea in Kp10- and C6-treated groups, indicating restored ovulation. C6 demonstrated equivalent efficacy to Kp10 in mitigating HPRL-induced reproductive dysfunctions, offering a promising alternative therapy. Future investigations should further explore the mechanistic advantages of C6, particularly its role in LH regulation, to optimize treatment strategies for HPRL-related reproductive disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.