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. 2022 Jan 10;20:12. doi: 10.1186/s12958-021-00878-y

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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