ArticleInternational journal of obesity (2005)2025
Agomelatine alleviates palmitic acid-induced mouse oocyte meiosis defects by restoring mitochondrial function.
Article in International journal of obesity (2005), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND/
objectivePalmitic acid (PA) is known to be elevated in the follicular fluid of women with obesity, negatively affecting female fertility. However, the mechanism by which PA exposure reduces female fertility is not fully understood, and how it can be treated requires further investigation.
methodsWe first established in vivo and in vitro models of mouse oocyte maturation at high concentrations of PA and determined the effects of treatment with agomelatine (Ago) which is a melatonin receptor agonist with antioxidant properties. We assessed oocyte maturation rates, spindle morphology and chromosome morphology, oxidative stress and apoptosis levels. Lastly, we examined energy levels, mitochondrial function, and mitochondrial synthesis-related protein expression levels.
resultsOur results showed that PA exposure disrupted spindle assembly and chromosome alignment, reduced microtubule stability, and impaired the meiotic maturation of oocytes. PA also disrupted mitochondrial function, leading to decreased ATP production, elevated Reactive Oxygen Species(ROS) levels, oxidative stress, and apoptosis. Remarkably, Ago supplementation promoted oocyte quality by restoring spindle/chromosome conformation, maintaining mitochondrial function, lowering ROS levels, and inhibiting apoptosis.
conclusionsThis study establishes that Ago ameliorates metabolic stress-induced oocyte deterioration through mitochondrial functional restoration, providing mechanistic insights into obesity-associated infertility. Importantly, our study identifies a potentially favorable drug for combating obesity-induced female infertility.
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