ArticleJournal of ovarian research2025
Exercise-diet intervention ameliorates but fails to fully reverse obesity-induced ovarian dysfunction: evidence spanning folliculogenesis to embryonic development.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Obesity is the culprit behind fatty acid-induced inflammation.Nutrition & metabolism · 2026Review
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
Abstract
Obesity, a globally prevalent chronic disease, disrupts systemic homeostasis and impairs female fertility, yet the mechanisms linking adipose dysfunction to ovarian reserve remain unclear. Using high-fat diet-induced obese C57BL/6 mouse models (HFD) and exercise-diet intervention models (SE group), we systematically evaluated obesity-associated reproductive deficits. Histomorphological analysis revealed that HFD mice exhibited ovarian atrophy, increased atretic follicles, and reduced primordial/antral follicle counts, which were partially restored by SE intervention. TEM demonstrated lipid droplet accumulation and mitochondrial heterogeneity in HFD ovaries, with residual vacuolization persisting despite SE-mediated improvement. Superovulation assays demonstrated reduced oocyte production in HFD mice, accompanied by impaired in vivo maturation and blastocyst formation. Immunofluorescence revealed abnormal spindle assembly and heterogeneous mitochondrial distribution in HFD oocytes, potentially associated with elevated ROS. Mechanistically, HFD downregulated folliculogenesis regulators (BMP-15, HIF-1α, PTEN/AKT/FoxO3) while upregulating metabolic stress markers (Chemerin, CMKLR1). Western blot confirmed reduced ovarian protein acetylation and BMP-15/HIF-1α expression in HFD mice, with partial recovery following exercise-diet intervention. These findings demonstrate obesity-induced dual impairments: mitochondrial-ROS dysfunction compromising oocyte competence and BMP-15/HIF-1α suppression disrupting follicular survival through PTEN-AKT-FoxO3 signaling. Although exercise-diet intervention improved metabolic parameters and oocyte quality, residual abnormalities highlighted irreversible impairments. Our study identifies obesity as a driver of ovarian aging and emphasizes the fertility-enhancing potential of combined exercise-diet intervention in obese female mice.
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.