Fig. 1
From: Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation
Altered molecular pathways of subcutaneous (SC) abdominal adipogenesis in polycystic ovary syndrome (PCOS) as a risk factor for lipotoxicity. In normal-weight PCOS women, exaggerated adipose stem cell (ASC) development to adipocytes occurs via androgen-independent mechanisms [23, 50]. Simultaneously, androgen excess inhibits early-stage adipogenesis, diminishes insulin-stimulated glucose uptake, promotes lipid storage and impairs catecholamine-stimulated lipolysis [31, 32, 35, 40, 47], favoring abdominal fat deposition and increased energy availability through hyperandrogenism and insulin resistance, respectively. These same traits are worsened in overweight/obese PCOS women who have greater preferential abdominal fat accumulation, hyperandrogenism, and systemic insulin resistance [2], along with impaired insulin suppression of lipolysis [2, 44], promoting ectopic lipid deposition and lipotoxicity [1]