Abstract
The complex nature of folliculogenesis regulation accounts for its susceptibility to maternal physiological fitness. In obese mothers, progressive expansion of adipose tissue culminates with severe hyperestrogenism and hyperleptinemia with detrimental effects for ovarian performance. Indeed, maternal obesity is associated with the establishment of ovarian leptin resistance. This review summarizes current knowledge on potential effects of impaired leptin signaling throughout folliculogenesis and oocyte developmental competence in mice and women.
Highlights
Obesity is a prevalent disease worldwide, usually associated with infertility
We demonstrated the establishment of leptin resistance in the ovary of diet-induced obese (DIO; abbreviations listed after the main text) mice after 16 weeks in comparison to 4 wk [6]
Folliculogenesis regulation is a complex process that depends on the crosstalk between local and systemic factors, accounting, for its vulnerability to maternal physiological fitness
Summary
Obesity is a prevalent disease worldwide, usually associated with infertility. Obesity has been shown to hamper oocyte maturation and quality [4] and embryo development [5], with reported long term effects and direct causality between obesity in the mother and prevalence of cardiovascular disease or cancer in the offspring. Increased levels of leptin signaling inhibitor suppressor of cytokine signaling (SOCS) 3 were observed already after 4 wk DIO [6] with potential implications for ovarian pathogenesis during early obesity. We consider how maternal obesity and, local changes in leptin signaling can affect the regulation of such transitions, debating potential outcomes for oocyte quality and early embryo development
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