作者: Abbott , Rogers , Dumesic , Levine
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摘要: Indian rhesus macaque nonhuman primate models for polycystic ovary syndrome (PCOS) implicate both female hyperandrogenism and developmental molecular origins as core components of PCOS etiopathogenesis. Establishing exploiting translational impact into the clinic, however, has required multi-year, integrated basic-clinical science collaborations. Paradigm shifting insight accrued from such concerted investment, leading to novel mechanistic understanding PCOS, including hyperandrogenic fetal peripubertal origins, epigenetic programming, altered neural function, defective oocytes embryos, adipogenic constraint enhancing progression insulin resistance, pancreatic decompensation type 2 diabetes, together with placental compromise, all contributing transgenerational transmission traits likely manifest in adult phenotypes. Our recent demonstration PCOS-related naturally (High T) macaques additionally creates opportunities employ whole genome sequencing enable exploration gene variants within human candidate genes models. This review will therefore consider model contributions various aspects pathophysiology, well benefits using compellingly close homologies genome, phenotype, development aging.