Abstract:: Obesity-related female infertility is a result of the intricate interplay between metabolic disorders and reproductive abnormalities. The Phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway is an important molecular mediator that translates insulin action, adipokine function, and ovarian physiology. In obesity, the aberrant regulation of protein and peptide mediators of this pathway, such as insulin, adipokines, gonadotropins, and inflammatory cytokines, results in dysfunctional follicular growth, hormonal dysregulation, and decreased endometrial receptibility. Recent studies indicate that modulation of the PI3K/AKT pathway may provide novel therapeutic strategies to manage both metabolic and reproductive complications of obesity. This article focuses on the mechanistic and clinical implications of PI3K/AKT pathway dysfunction in obesity-related female infertility.
Rathod et al. (Mon,) studied this question.
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