In vitro embryo production depends on high-quality oocytes. Compared with in vivo matured oocytes, in vitro oocytes undergo precocious meiotic resumption, thus compromising oocyte quality. C-type natriuretic peptide (CNP) is a follicular factor maintaining meiotic arrest. Thus, CNP-pretreatment has been widely used to improve the in vitro maturation (IVM) of oocytes in many species. However, the efficacy of this strategy has remained unsatisfactory in porcine oocytes. Here, by determining the functional concentration and dynamics of CNP in inhibiting spontaneous meiotic resumption, we improved the current IVM system of porcine oocytes. Our results indicate that although the beneficial effect of the CNP pre-IVM strategy is common among species, the detailed method may be largely divergent among them and needs to be redesigned specifically for each one. Focusing on the overlooked role of cumulus cells surrounding the oocytes, we also explore the mechanisms relevant to their beneficial effect. In addition to oocytes per se, the enhanced anti-apoptotic and anti-oxidative gene expression in cumulus cells may contribute considerably to improved oocyte quality. These findings not only emphasize the importance of screening the technical parameters of the CNP pre-IVM strategy for specific species, but also highlight the critical supporting role of cumulus cells in this promising strategy.

Parturient paresis remains a major economic challenge in global ruminant production, causing acute periparturient hypocalcemia and predisposing high-yielding animals to a cluster of secondary pathologies. Traditional narratives often treat regulatory pathways in isolation, whereas this review synthesizes multi-organ endocrine networks to address the kinetic dyssynchrony between mammary calcium drain and homeostatic recruitment velocity. Beyond the classical parathyroid hormone–vitamin D axis, we integrate the mammary–gut–bone axis into a unified endocrine model, highlighting the critical role of the serotonin–parathyroid hormone-related protein rheostat for skeletal mineral mobilization and the fibroblast growth factor 23–Klotho axis in prepartum phosphorus-induced feedback suppression. We evaluate the molecular mechanisms underlying target-organ receptor resistance, driven by vitamin D receptor downregulation and epigenetic aging, which precipitate homeostatic feedback failure. Regarding clinical management, this synthesis contrasts reactive parenteral interventions with proactive nutritional priming strategies, such as negative dietary cation–anion difference acidification, zeolite-based gastrointestinal binders, and exogenous vitamin D or 5-hydroxytryptophan supplementation. Additionally, the role of microbiota-derived short-chain fatty acids in gut-bone communication and the potential of genomic selection to breed livestock with heritable metabolic resilience are explored. Ultimately, this comprehensive framework emphasizes a paradigm shift from emergency treatment to precision nutritional and genetic prophylaxis to mitigate PP across diverse ruminant species.