Early neuroendocrine signatures of polyendocrine metabolic ovarian syndrome risk: Pubertal programming, social brain signals, and novel therapeutic targets.
AI interpretation is pending for this paper.
Open original publication →What the AI sees
Not AI summarized yet.
Research significance
Pending deeper interpretation.
Source abstract
Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is increasingly recognized as a disorder with developmental origins, yet its early neuroendocrine antecedents during puberty remain poorly understood. While most diagnostic frameworks apply post-menarche, growing evidence suggests that PMOS risk may be programmed well before clinical onset through alterations in central neuroendocrine pathways that emerge during the pubertal transition. In this review, we examine the concept of pubertal neuroendocrine programming in girls at risk for PMOS, with a particular focus on kisspeptin-GnRH dysregulation, central metabolic signaling, and the emerging role of oxytocin in modulating reproductive and behavioral outcomes. We propose that early disturbances in the integration of reproductive, metabolic, and social neuroendocrine circuits contribute to the trajectory toward PMOS. Special attention is given to the "social brain," including oxytocinergic pathways, which may influence stress sensitivity, emotional eating, and pubertal tempo; underexplored but potentially modifiable dimensions of PMOS risk. By synthesizing data from basic science, translational models, and adolescent cohorts, we outline neuroendocrine signatures of early PMOS vulnerability and evaluate their potential as biomarkers and therapeutic targets. Finally, we discuss opportunities for intervention during the pubertal window, including lifestyle, behavioral, and central nervous system-targeted therapies. Understanding how the brain orchestrates puberty in at-risk individuals may unlock new strategies for preventing PMOS before it fully manifests, shifting the clinical focus from late diagnosis to early modulation.