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Fig. 2 | Reproductive Biology and Endocrinology

Fig. 2

From: Polycystic ovary syndrome as a plausible evolutionary outcome of metabolic adaptation

Fig. 2

Metabolic adaptation in polycystic ovary syndrome. Inherently accelerated adipogenesis, along with enhanced intracellular aldo-ketoreductase type 1C3-mediated testosterone generation, in subcutaneous (SC) abdominal adipose promotes lipid storage (through increased lipogenesis and decreased lipolysis) to protect against insulin resistance. Simultaneously, hyperandrogenemia accompanies preferential accumulation of highly-lipolytic intra-abdominal fat with an opposite effect. As a result, SC fat storage counterbalances increased circulating glucose and free fatty acid (FFA) availability for energy use. When energy intake exceeds fat storage capacity, excess fatty acid influx into skeletal muscle and liver promotes lipotoxicity through ectopic lipid accumulation accompanied by oxidative stress, insulin resistance and inflammation in non-adipose tissue

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